Preparation of cells

Abstract

The present invention relates to granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell comprises: (a) increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or (b) decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. Also provided are cells, methods for producing the same, uses of the same, and kits comprising the same.

Description

[0001] PREPARATION OF CELLS FIELD OF THE INVENTION The invention relates to methods of preparing cells for therapeutic use to produce a population of progenitor cells (for example, the invention relates to methods of producing a population of granulocyte progenitor cells and methods of producing granulocyte precursor cells and use thereof for treating a disease, e.g. cancer). BACKGROUND Cancer is a leading cause of morbidity and mortality worldwide, with cancer incidence increasing annually in developed countries. The World Health Organisation stated that in 2012 alone there were approximately 14 million new cancer cases (and 8.2 million associated deaths), with a projected rise to 22 million cases over the next two decades. Current therapeutic strategies include combinations of surgery, radiation, and cytotoxic chemotherapy, however many of these treatments are ultimately ineffective and associated with harmful side-effects. Host therapeutic immune responses often involve several types of immune cell and play a vital role in the body’s fight against cancer, infections and virtually all other diseases. However, a subject’s native therapeutic immune response is not always enough to eradicate disease. For example, tumours may be adapted to be immunologically “cold”, and may create an immunosuppressive tumour microenvironment (TME) that can render native anti- tumour therapeutic immune responses ineffective. Chimeric antigen receptor T cell (CAR-T cell) therapy has met with some success. However, CAR-T cell therapy has been shown to have limited efficacy in the treatment of solid tumours. Thus, there is a need for cell therapies that treat solid tumours, such as in lung cancer, cervical cancer and head and neck cancer. For optimal tumour eradication (e.g. in cancer), it is advantageous if a variety of different types of immune cells work together. However, in some cases, a subject’s own immune cells may be defective meaning there is a need for a variety of different types of immune cells from an alternative source. There are currently difficulties in manufacturing such cell combinations. Additionally or alternatively, such conventional cell combinations may have adverse immunogenic effects. It would be advantageous to have a cell therapy capable of promoting proliferation and / or activation of other immune cells present in a subject, thereby reversing the defective nature of a subject’s immune cells. Conventional Leukocyte Infusion Therapy (LIFT) is carried out using apheresis for direct transfer of granulocytes taken from the donor to the cancer patient. Conventional approaches currently used in the clinic are not practical or scalable for use as a credible and sustainable source of cancer therapeutic. First, granulocytes such as neutrophils have a very limited shelf-life (typically less than 24 hours) making them difficult to store. Secondly, apheresis requires approximately 5 (very rare) donors in order to acquire the required cell number. Thirdly, to avoid an allogeneic immune response from repeat exposure, the same donors cannot be used in a subsequent administration, thus requiring an increased pool of appropriate donors. Fourthly, it cannot be realistically expected that donors will be available on request, or willing to provide an endless source of granulocytes for the LIFT procedure. Thus, there exists a problem associated with the economic viability, sustainability, and scalability of conventional LIFT therapies. The present invention provides a solution to at least one of the problems described above. SUMMARY OF THE INVENTION In a first aspect, the invention provides a method of preparing granulocytes, or precursors thereof (preferably granulocyte precursors), for therapeutic use, the method comprising culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte progenitor cells comprise the presence of: • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs. In a second aspect, the invention provides a method of preparing cells (e.g. granulocytes, or precursors thereof, preferably granulocyte precursors) for therapeutic use, the method comprising culturing a population of granulocyte progenitor cells in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (e.g. preferably granulocyte precursors), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. In a third aspect, the invention provides a method of preparing cells (e.g. granulocytes, or precursors thereof, preferably granulocyte precursors) for therapeutic use, the method comprising: culturing a population of stem cells in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte precursor cells comprise the presence of: • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells (HSC); to produce the population of granulocyte progenitor cells and further comprising culturing granulocyte progenitor cells of this (said) population in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursors), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. In a fourth aspect, the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursors), wherein: • at least 50% of the cells of the population express CD11b, • at least 50% of the cells of the population express CD15, • at least 50% of the cells of the population express CD64, • at least 50% of the cells of the population express CD89, • at least 50% of the cells of the population express CXCR2, • at least 50% of the cells of the population express neutrophil elastase, • less than 50% of the cells of the population express CD14, • less than 50% of the cells of the population express CD19, • less than 50% of the cells of the population express CD3, • less than 50% of the cells of the population express CD34, • less than 50% of the cells of the population express CD66b, • less than 50% of the cells of the population express CD68, • less than 50% of the cells of the population express CXCR4, and / or (preferably and) • less than 50% of the cells of the population express HLA-DR. In a fifth aspect, the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursors), comprising granulocytes, or precursors thereof (preferably granulocyte precursors), wherein: • at least 50% of the cells of the population express CD64; and / or (preferably and) • at least 50% of the cells of the population express CD89; and / or neutrophil elastase. In a sixth aspect, the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursors), comprising granulocytes, or precursors thereof (preferably granulocyte precursors), wherein: • at least 50% of the cells of the population express CD64; • at least 50% of the cells of the population express CD89; and / or • at least 50% of the cells of the population express neutrophil elastase. In a seventh aspect, the invention provides a population of neutrophils, or precursors thereof (preferably granulocyte precursors), comprising neutrophils, or precursors thereof (preferably granulocyte precursors), expressing neutrophil elastase, and wherein at least 50% of the cells of the population express CD64; and / or CD89. Except for where context requires otherwise, references in the present disclosure to “populations of the invention” or “populations of cells of the invention”, or to “cells of the invention”, should respectively be taken as encompassing populations of any of the fourth to seventh aspects of the invention, or constituent cells of such populations. Except for where context requires otherwise, references in the present disclosure to “populations of the invention” or “populations of cells of the invention”, or to “cells of the invention”, should respectively be taken as encompassing populations of any of the fourth to seventh aspects of the invention, or constituent cells of such populations as well as any populations of granulocytes or precursors thereof (preferably granulocyte precursors) or granulocyte precursor cells obtainable by the methods of the inventions. In an eighth aspect, the invention provides a pharmaceutical composition comprising a population of cells of the invention. Suitably, the population of cells may be in accordance with any of the fourth to seventh aspects of the invention In a ninth aspect, the invention provides a population of cells according to any of the fourth to seventh aspects of the invention, or a pharmaceutical composition according to the eighth aspect of the invention, for use as a medicament. In a tenth aspect, the invention provides a method of treating a disease or condition comprising providing a therapeutically effective amount of a population of cells of the invention, or of a pharmaceutical composition of the invention, to a subject in need of such treatment. Suitably, the population of cells may be in accordance with any of the fourth to seventh aspects of the invention. Suitably, the pharmaceutical composition of the invention may comprise a population of cells in accordance with any of the fourth to seventh aspects of the invention. In an eleventh aspect, the invention provides the use of a population of cells of the invention, or a pharmaceutical composition of the invention, in the manufacture of a medicament. Suitably, the population of cells may be in accordance with any of the fourth to seventh aspects of the invention. Suitably, the pharmaceutical composition of the invention may comprise a population of cells in accordance with any of the fourth to seventh aspects of the invention. In one aspect, the invention provides a granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell comprises: a. increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or b. decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one aspect, the invention provides a method of preparing cells (e.g. granulocytes, or precursors thereof, preferably granulocyte precursor cells) for therapeutic use, the method comprising: culturing a population of stem cells (preferably HCSs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte precursor cells comprise the presence of: • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs; to produce the population of granulocyte progenitor cells, and further comprising culturing the granulocyte progenitor cells of said population in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. In one aspect, the invention provides a granulocyte or granulocyte precursor (preferably a granulocyte precursor cell or a population thereof) obtainable (or obtained) by the methods of the invention. In one aspect, the invention provides a granulocyte, or granulocyte precursor (preferably a granulocyte precursor cell or a population thereof). In one aspect, the invention provides a granulocyte or precursor thereof (preferably a granulocyte precursor cell or a population thereof) obtainable (or obtained) by the methods of the invention, wherein the granulocyte or granulocyte precursor is a (in vitro differentiated) granulocyte precursor cell comprising: a) increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or b) decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one aspect, the invention provides a pharmaceutical composition comprising a granulocyte or precursor thereof (preferably a granulocyte precursor cell(s)) as taught herein or a population of granulocytes or precursor thereof (preferably a population of granulocyte precursor cells) as taught herein. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein for use as a medicament. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in the manufacture of a medicament. In one aspect, the invention provides a method for treating a disorder comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein for use in treating cancer. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in the manufacture of a medicament for treating cancer. In one aspect, the invention provides for a method for treating cancer comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in combination with a CAR-T cell. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in combination with an antibody selected from: Cetuximab, Rituximab, Daratumumab, Tafasitamab, Obinutuzumab, Ofatumumab, Alemtuzumab, Blinatumomab, Lynozyfic, Panitumumab, Bevacizumab, Ramucirumab, Denosumab, Dinutuximab, and Elotuzumab, preferably Cetuximab. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in combination with an immune check point inhibitor selected from: Nivolumab, Ipilimumab, Pembrolizumab, Cemiplimab, Durvalumab, Atezolizumab, Relatlimab, Dostarlimab, Avelumab, Tislelizumab, Toripalimab, Sugemalimab, Camrelizumab, and Tremelimumab, preferably Nivolumab. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein for use in treating an infection. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in the manufacture of a medicament for treating an infection. In one aspect, the invention provides a method for treating an infection comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein for use in treating an autoimmune disease. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein in the manufacture of a medicament for treating an autoimmune disease. In one aspect, the invention provides for a method for treating an autoimmune disease comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably granulocyte precursor cell(s)) as taught herein or a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition as taught herein. In one aspect, the invention relates to a kit comprising: a) a granulocyte or granulocyte precursor as taught herein (preferably granulocyte precursor(s)) or a pharmaceutical composition thereof; and / or b) a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or a pharmaceutical composition thereof; and c) optionally instructions for use of the same in medicine, e.g. in treating cancer and / or an infection and / or an autoimmune disorder. In one aspect, the invention relates to a kit comprising: a) a granulocyte or granulocyte precursor as taught herein (preferably granulocyte precursor(s)) or a pharmaceutical composition thereof; and / or b) a population of granulocytes or granulocyte precursors (preferably a population of granulocyte precursor cells) as taught herein or pharmaceutical composition thereof; and c) instructions for use of the same in medicine, e.g. in treating cancer and / or an infection and / or an autoimmune disorder. BRIEF DESCRIPTION OF THE DRAWINGS Figure 1: Cancer cell killing activity of A549 cells, either genetically modified ‘in house’ or commercially available ‘A549 EPC’ for granulocytic cells produced by methods of the invention (“0.4c 1e6 – C (E4) Stemline II” and “0.4d 1e6 – C (E4) Stemline II”) versus comparator cells. Results of the study are set out in Example 7. Figure 1A: Cancer killing activity of granulocyte precursor cells obtained by a method of the invention using the culture medium v0.4d (“IMANs (v.04d)” was compared to that of granulocyte precursor cells (“IMANs (v0.3d)” referred to as “comparator cells”) obtained by a method using the culture medium v0.3c). Both methods used HSCs from the same donors as the starting material. A549 (NSCLC) cancer cells were used in the in vitro luciferase-based cytotoxicity assay. The results are expressed as fold changes in cancer killing activity of granulocyte precursor cells obtained by a method of the invention using the culture medium v0.4d (“IMANs (v.04d) relative to the comparator cells (granulocyte precursor cells (“IMANs (v0.3d)”). The data show that the granulocyte precursor cells obtained by a method of the invention using the culture medium v0.4d (“IMANs (v.04d)) exhibit a 1.4- to 2.4-fold increase in cancer-killing activity compared to the comparator cells (granulocyte precursor cells (“IMANs (v0.3d)”), which were obtained by a method using the culture medium v0.3c. Figure 2: Cell count for various cell types (PBMCs – Figure 2A; granulocytic cells of the invention (granulocytic cells) – Figure 2B; CD3+ cells – Figure 2C; NK cells – Figure 2D) when in co-culture with PBMCs cultured with comparator cells or cells produced by methods of the invention (0.4c; 0.4d). Results of the study are set out in Example 8. Figure 3: Cell viability (Figure 3A) and cell count (Figure 3B) of granulocytic cells of the method of invention (IMAN; 0.4d), across a 10 day period post-thaw when cultured with UM729, versus reference cells and cells of a previous method. The cell viability (Figure 3C) and cell count (Figure 3D) of granulocytic cells of the invention when cultured with additional G-CSF supplementation is also shown. Results of the study are set out in Example 9. Figure 4: Percentage of the granulocytic cell population produced by methods of the invention (granulocytic cells) expressing a specific marker expression profile: CD15+ (myeloid committed – Figure 4A), CD15-;CD11b+;HLA-DR- (lineage (lin) committed – Figure 4B), CD15-;CD11b-;HLA-DR+ (progenitors – Figure 4C), and CD15-;CD11bHi;HLA-DRHi (“off target” differentiation – Figure 4D), versus reference cells and comparator cells across a 10 day period. Figures 4E-H show the same as above, but with additional G-CSF supplementation. Results of the study are set out in Example 10. Figure 5: Percentage of the granulocytic cell population produced by methods of the invention (granulocytic cells) expressing neutrophil elastase (Figure 5A), MPO (Figure 5B), and Cathepsin G (Figure 5C) versus reference cells and comparator cells across a 10 day period. Figures 5D-F show the same as above, but with additional G-CSF supplementation. Results of the study are set out in Example 11. Figure 6: Cell count for the granulocytic cell population produced by methods of the invention (granulocytic cells - Figure 6A) and PBMCs (Figure 6B) when in co-culture over a 2 day period. Figures 6C and 6D show the same as above, but with additional G-CSF supplementation. Results of the study are set out in Example 12. Figure 7: Flow cytometry data comparison of comparator cells (Figure 7A – 7F), versus granulocytic cells produced by methods of the invention (Figure 7G – 7L). Results of the study are set out in Example 13. %P indicates percentage of parent gate. Results of the study are set out in Example 13. Figure 8: Flow cytometry data comparison for conditions with the inclusion of a pyrimido- [4,5-b]-indole derivative in methods of the invention (+UM729) versus comparator cells (- UM729) when cultured in the presence of two different types of cell culture media (IMDM, and Stemline II). %P indicates percentage of the parent population. %P indicates percentage of parent gate. Results of the study are set out in Example 14. Figure 9: Cancer cell killing activity for granulocytic cells produced by methods of the invention, cultured in the presence of the pyrimido[4,5-b]-indole derivative UM171, at an effector:target (E:T) ratio of 20:1 versus 40:1 of A549 cells. The donor used for this study was NTP016. Results of the study are set out in Example 14. Figure 10: Percentage expression of CD34, CD13, HLA-DR, CD71, CD15, CD49d, CD33, CD38, and CD45RA (Figure 10A) across the live cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD11b, HLA-DR, CD64, CXCR4, CD32, CD89, and CD40 (Figure 10B) across the CD15- cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD11b, HLA-DR, CD64, CXCR4, CD32, CD89, and CD40 (Figure 10C) across the CD15+ cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD64, CXCR4, CXCR2, CD32, CD89, and CD40 (Figure 10D) across the live cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD11b-, 4-1BBL, CD40L, OX40L, CD54, FasL, and CD18 (Figure 10E) across the CD15+ cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD11b-, 4-1BBL, CD40L, OX40L, CD54, FasL, and CD18 (Figure 10F) across the CD15- cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). Percentage expression of CD11b, 4-1BBL, CD40L, OX40L, CD54, FasL, and CD18 (Figure 10G) across the live cells produced on expansion day 8 (E8) across three different donors (NTP016, NTP005, NTP006-2). This figure has a further description in Example 16. Figure 11: Expression of 3 activation markers (4-1bb (Figure 11A), CD69 (Figure 11B) and CD25 (Figure 11C) of CAR-T cells when cultured on their own or in co-culture with granulocytic cells (IMANs) at different concentrations of conditions. Results of the study are set out in Example 17. Figure 12: Cell count (Figure 12A) of CAR-T cells when cultured on their own, in co-culture with cancer cells (SK-OV-3), or in co-culture with cancer cells (SK-OV-3) and granulocytic cells (IMANs). Figure 12B shows the percentage CAR expression of the cell population when cultured on their own, in co-culture with cancer cells (SK-OV-3), or in co-culture with cancer cells (SK-OV-3) and granulocytic cells (IMANs). Results of the study are discussed in Example 18. Figure 13: Expression of CD25 (Figure 13A), CD69 (Figure 13B), 4-1bb (Figure 13C), CD25 (Figure 13D), CD69 (Figure 13E), and 4-1bb (Figure 13F). Figure 14: Cell count (Figure 14A) of CAR-T cells when in co-culture with cancer cells (SK- OV-3), or in co-culture with cancer cells (SK-OV-3) and granulocytic cells (IMANs). Figure 14B shows the percentage CAR expression of the cell population when cultured on their own, in co-culture with cancer cells (SK-OV-3) and granulocytic cells (IMANs). Results of the study are discussed in Example 20. Figure 15: Tumour cell count over time (hours) for SK-OV-3 cancer cells alone (‘target alone’), a co-culture of IMAN and SK-OV-3 at a ratio of 10:1, a co-culture of IMAN and CAR- T cells at a ratio of 10:1, and a co-culture of CAR-T, IMAN, and SK-OV-3 at a ratio of 10:10:1 (Figure 15A). The tumour cell count from 60 hours onwards is shown in Figure 15B, as SK- OV-3 cancer cells (200,000) were added to the cultures at 72 hours. Results are set out for this study in Example 21. Figure 16: The percentage live T cells in the presence of a range of IMAN:T-cell ratios are shown in Figure 16A after 96 hours of culture. The expression of activation markers as a percentage of the T cell population for 4-1bb (Figure 16B), CD25 (Figure 16C), CD69 (Figure 16D), and OX40 (Figure 16E) when in co-culture with IMANs, are shown after 96 hours of culture. Results are discussed in Example 22. Figure 17: Percentage expansion of T cells in co-culture with SK-OV-3 cancer cells over a 96 hour culture period is assessed in Figure 17A, comparing CAR-T cells alone versus CAR-T cells in co-culture with IMANs. In Figure 17B, the SK-OV-3 cancer cell count is shown across the same 96 hour period. Results are discussed in Example 23. Figure 18: Table of versions of the method across expansion day 0 – day 8 (E0-E8) and differentiation (E8D0 – E8D4 / E8D5) for previous methods (0.3c), and methods of the invention (0.4c and 0.4d). Figure 19: Chemical structure of pyrimido-[4,5-b]-indole derivative, methyl 4-((3-(piperidin-1- yl)propyl)amino)-9H-pyrimido[4,5-b] indole-7-carboxylate, referred to as UM729. Figure 20: Chemical structure of pyrimido-[4,5-b]-indole derivative, (1r,4r)-N1-(2-benzyl-7-(2- methyl-2H-tetrazol-5- yl)-9H-pyrimido[4,5-b]indol-4-yl)cyclohexane-1,4-diamine, referred to as UM171. Figure 21 illustrates the donor selection process. Whole blood from individual donors (each donor is represented by a distinct pattern / dot) was collected and processed to isolate neutrophils for use in the in vitro luciferase-based cytotoxicity assay using A549 (NSCLC) cancer cells. All neutrophil isolations resulted in >98% CD15+CD66b+cells out of the viable cells. Increased cancer cell killing activity was observed with increasing neutrophil to cancer cell (effector to target) ratio. The donors were selected based on their consistent demonstration of their neutrophil capacity to kill cancer cells (percentage (%) lysis) above the dataset mean across all E:T ratios. The selected donors (n=5) meeting this criterion can be seen as an individual dot (Panel (A)) or as a distinct pattern (Panel (B)) above the dataset mean, which can be followed across all E:T ratios via their respective distinct lines. Panel (C) shows the percentage (%) of lysis observed in the same in vitro luciferase-based cytotoxicity assay using positive controls supT1 and staurosporine (known cytotoxic agents) at different E:T ratios or concentrations. Each individual dot / pattern represents one experimental run. The dotted lines in panel B indicate the dataset mean. Figure 22: Overview of the experimental design. Figure 23: Figure 23 shows the results of a cytotoxicity assay evaluating a combination therapy consisting of granulocyte precursor cells obtained by a method of the invention using the culture medium v0.4d (“IMANs (v.04d)”) in combination with an antibody (a biosimilar version of Cetuximab, which is an anti-hEGFR IgG1 monoclonal antibody). The Cetuximab biosimilar was tested at 3 different concentrations, namely 8 ng / mL, 40 ng / mL, and 200 ng / mL. An IgG1 isotype control antibody, which lacks therapeutic efficacy, was included as a negative control. FaDu cancer cells were used as target cells. The results show that target cell (FaDu cancer cells) killing was significantly enhanced in the presence of the antibody compared to the isotype control, indicating that the observed cytotoxicity is specifically mediated by antibody-dependent cellular cytotoxicity (ADCC). Moreover, target cell killing increased in a dose-dependent manner with escalating concentrations of the ADCC- promoting antibody (Cetuximab biosimilar). Figure 24: Overview of the TruTumor histoculture model Figure 25: Figure 25 shows the results of a cytotoxicity assay, using the TruTumor histoculture model, evaluating a combination therapy consisting of granulocyte precursor cells obtained by a method of the invention using the culture medium v0.4d (“IMANs (v.04d)”) in combination with a check point inhibitor (Nivolumab). DETAILED DESCRIPTION OF THE INVENTION The invention is based, at least in part, on the inventors’ development of novel and advantageous methods for the preparation of granulocytes, or precursors thereof (preferably granulocyte precursors), that are suitable for use in a number of therapeutic applications. The inventors have previously defined a group of cells (that they have termed “Immunomodulatory Alpha Neutrophils” – IMANs) that have biological activities that make them useful in a range of therapeutic applications. The methods of the present invention provide improved methods for the preparation of such cells, and the populations of granulocytes, or precursors thereof (preferably granulocyte precursors), or neutrophils, or precursors thereof, (collectively referred to as the “cells of the invention”) defined herein, which may be prepared by the methods of the invention, provide improved examples of such cells for therapeutic use. Merely by way of example, the cells of the invention may be used in the treatment of diseases, such as cancer, or of infections. The cells possess cytocidal activity (e.g. cancer killing activity), by which they can kill pathological cells, such as cancer cells or infected cells, to provide a therapeutic effect. Furthermore, the cells of the invention possess immunomodulatory activity, by which they can modify an immune response (for example by amplifying the immune response) as an alternative or additional route by which they can provide a therapeutic effect. The Examples illustrate that cells of the invention demonstrate enhanced cancer cell killing activity as compared to granulocytic cells (e.g. natural (wild type) granulocytic cells such as granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vivo or granulocytic cells such as granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vitro and produced by alternative methods (e.g. different from the method of the present invention). It will be appreciated that this property will offer clear advantages in the treatment of cancer. Since this anti-cancer activity is associated with the cytocidal properties of the cells of the invention, the skilled person will recognise that it is also to be expected that these cells (e.g. granulocyte precursor cells) will offer corresponding advantages in their ability to kill other pathological cells, such as infected cells. The cells of the invention also demonstrate increased persistence (e.g. enhanced ability to survive and maintain their function) in vitro and in vivo following administration to an organism (e.g. mice), as compared to alternative granulocytic cells (e.g. natural (wild type) granulocytic cells such as granulocyte precursors of an equivalent developmental stage that have been differentiated in vivo or granulocytic cells such as granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vitro using an alternative methods). Increased persistence of the cells of the invention facilitates the accumulation of therapeutically effective quantities of such cells, and may enable longer lasting therapy. The cells of the invention also demonstrate enhanced expression of markers associated with commitment to the neutrophil lineage. It will be appreciated that neutrophils are particularly active in the response to diseases (such as cancer) or infections. The inventors have also demonstrated that cells of the invention contain increased effector granule content as compared to alternative granulocytic cells (e.g. natural (wild type) granulocytic cells such as granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vivo or granulocytic cells such as granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vitro and produced by alternative methods. In particular increased neutrophil elastase and myeloperoxidase, constituents of effector granules known to play key roles in granulocytes’ anti-tumour activity and ability to fight infections. This increase in effector granule constituents is also noted at early timepoints, consistent with when such activity is required from cell therapies administered to a patient. The cells of the invention promote expansion of PBMCs in culture. This property points to their ability to promote and organise an effective immune response in recipients, which will be expected to yield therapeutic benefits in practice. The cells of the invention demonstrate high expression of CD89, a modulator of inflammation that may have pro- or anti-inflammatory activity in vivo. This is consistent with an immunomodulatory role for the cells of the invention, which is further demonstrated by their ability to promote activation of immune cells such as T cells. In this regard, the inventors have shown that the cells of the invention offer particular benefits in combination with cells that may be used in adoptive immunotherapy, such as CAR-T cells. As demonstrated in the Examples, the cells of the invention are able to increase activation of CAR-T cells in response to the presence of cancer cells. They also increase CAR-T cell numbers and the proportion of cells expressing CARs (overcoming cancer-mediated downregulation of CAR expression) and promote CAR-T cell survival. The data generated by the inventors also suggest (without wishing to be bound by theory) that the cells of the invention may be able to overcome T cell exhaustion when used as a combination therapy with T cells. The inventors have also shown that the cells of the invention offer particular benefits in the context of a combination therapy, such as for instance, when the cells (preferably granulocytes precursor cells) of the invention are used in combination with an antibody (e.g. Cetuximab) or used in combination with an immune check point inhibitor (e.g. Nivolumab). As demonstrated in the Examples, the cells of the invention were shown to enhance the therapeutic effects of an antibody (via ADCC activity) and a check point inhibitor, resulting in greater, more potent cancer killing activity. One of the notable features of the methods of the invention is their use of a pyrimido-[4,5-b]- indole derivative that promotes the expansion of hematopoietic stem cells (HSC), as part of the culture condition during the “expansion phase”. This class of compounds is also known to promote the retention of “stemness” in stem cells cultured in their presence. Surprisingly, the inventors have found that methods employing these compounds give rise to cells of the invention that have increased cytocidal activity (e.g. cancer killing activity) for target cells, such as cancer cells. This is surprising as properties of the granulocyte populations (e.g. granulocyte precursor populations) produced by the methods of the invention would be expected to be more associated with differentiation along advantageous lines established during the differentiation phase, rather than as a result of increased stemness (i.e. a lack of differentiation). Furthermore, the inventors have identified that the commercially available pyrimido-[4,5-b]- indole derivative UM171 offers particular advantages in use. Cells (e.g. granulocyte precursor cells)produced by methods of the invention employing UM171 have elevated cancer cell killing activity as compared to cells (e.g. granulocyte precursor cells) produced in methods utilising an alternative pyrimido-[4,5-b]-indole derivative. Methods of the invention increase homogeneity of the cell product produced. This is advantageous in producing a consistently effective therapeutic agent (e.g. contributes to improve batch to batch consistency). The methods of the invention also increase yield of live cells (e.g. granulocyte precursor cells) as compared to protocols known to date. Preferably, progenitor cells are granulocyte progenitor cells, more preferably human granulocyte progenitor cells. The invention will now be defined further with reference to the following paragraphs, which include definitions that may be helpful in the understanding of the invention. Methods of preparing cells for therapeutic use The first, second and third aspects of the invention each relate to methods of preparing cells for therapeutic use. Methods of the invention may employ stem cells (e.g. HSC), which undergo expansion to produce a population of granulocyte progenitor cells, and / or granulocyte progenitor cells that undergo differentiation into granulocytes, or precursors thereof (preferably granulocyte precursors). The methods of the invention use cell culture conditions (including constituents of the cell culture media, supplements, such as cytokines, and selected times in culture) that promote expansion or differentiation as required. Suitable embodiments of the cells (e.g. granulocyte precursor cells) and cell culture conditions are set out further below. Advantageously, the methods of the invention use cell culture conditions (including constituents of the cell culture media) that are free of animal-derived products. Existing in vitro methods for producing granulocytes (e.g. neutrophils) and precursors thereof (e.g. granulocyte precursors) suffer certain limitations including the production of low yield of granulocytes (e.g. neutrophils) and precursors thereof (e.g. granulocyte precursors), immature or nonfunctional granulocytes (e.g. neutrophils) and precursors thereof, low cell viability and / or occurrence of contaminants (impurities) such as undesired cell types (e.g. cells of a lineage that is not of interest) and / or culture debris (dead cells). Moreover, existing in vitro methods suffer from low throughput, limited scalability, low GMP or regulatory compliance, and they often exhibit high batch-to-batch variability, which complicates product release and market entry. The present invention provides a solution to at least some of these limitations. The following paragraphs set out details of useful embodiments of the methods of the first, second and third aspects of the invention. These include useful embodiments of the stem cells (e.g. HSC) or granulocyte progenitor cells that may be used as starting material, and the cell culture conditions that may be employed. Characteristics of the populations of granulocytes, or precursors thereof (e.g. granulocyte precursors), produced by the methods of the invention are considered in more detail elsewhere in the specification. Stem cells suitable for use in the methods of the invention The term “stem cell” as used herein encompasses any cell that is capable of differentiating (preferably that differentiates) into a population of granulocyte progenitor cells able to give rise to granulocytes or precursors thereof, or neutrophils, or precursors thereof. Suitably, the term “stem cell” may encompass totipotent, pluripotent, multipotent, or unipotent cells. The “stem cell” may be a natural stem cell or an artificial stem cell. In a suitable embodiment a natural stem cell may be a cell of the haematopoiesis pathway or a cell equivalent thereto. Thus, in a suitable embodiment the term “stem cell” encompasses a haematopoietic stem cell (HSC) capable of differentiating (preferably that differentiates) into a granulocyte progenitor cell that is itself capable of differentiating (preferably that differentiates) into a granulocyte, or precursor thereof (preferably a neutrophil, or precursor thereof). Preferably, the stem cell (e.g. HSC) differentiates into a granulocyte progenitor cell that itself differentiates into a granulocyte precursor cell. In a preferred embodiment, the stem cell is an HSC. More preferably, the stem cell is a human HSC. Further sources of natural stem cells (e.g. HSC), include, without limitation, include cord blood and mobilized blood. Stem cells from such sources represent suitable stem cells for use in the methods of the invention. A granulocyte or precursor thereof (e.g. granulocyte precursors) may be derived from an artificial stem cell which is an induced pluripotent stem cell (iPSC) or a cell equivalent thereto, preferably a human iPSC. A granulocyte progenitor cell may be derived from an artificial stem cell which is an induced pluripotent stem cell (iPSC) or a cell equivalent thereto, preferably a human iPSC. A granulocytes or precursor thereof (preferably granulocyte precursor cells) may be derived from sources of natural stem cells. In a preferred embodiment, the natural stem cell is an HSC obtained from a human donor selected according to the method as taught herein. A granulocyte progenitor cell may be derived from sources of natural stem cells. In a preferred embodiment, the natural stem cell is an HSC obtained from a human donor selected according to the method as taught herein. In a suitable embodiment a population of granulopoietic cells is derived from an artificial stem cell which is an induced pluripotent stem cell (iPSC) or a cell equivalent thereto. In a suitable embodiment, an iPSC is obtainable from a somatic cell, such as a somatic cell of a donor. Generation of iPSCs is a well-known technique in the art, see Yu et al (2007), Science, 318:1917-1920 the teaching of which is incorporated herein by reference. In another embodiment, an iPSC is obtainable from a stem cell (e.g. obtainable from a donor), such as from a stem cell of the hematopoietic pathway. Preferably an iPSC is obtainable from a hematopoietic stem cell or a precursor cell described herein. In a suitable embodiment, a stem cell is a nuclear transfer embryonic stem cell (NT-ESC) or equivalent thereto. In a suitable embodiment, an NT-ESC is obtainable by injecting the nucleus of a cell from the donor into an egg cell from which the original nucleus has been removed. Generation of NT-ESCs is a well-known technique in the art, see Tachibana M, Amato P, Sparman M, et al (2013), Cell, 154(2): 465-466 the teaching of which is incorporated herein by reference. A suitable stem cell (e.g. HSC, preferably an HSC derived from a donor selected according to the method as taught herein) may be immortalised. The person skilled in the art is familiar with immortalisation techniques, which include inter alia introduction of a viral gene that deregulates the cell cycle (e.g. the adenovirus type 5 E1 gene), and artificial expression of telomerase. Immortalisation advantageously allows for the preparation of a cell line which can be stably cultured in vitro. Thus, in one aspect the invention provides an immortalised cell line obtainable (e.g. obtained) from a selected stem cell, as well as a stable stem cell culture. Suitably an immortalised cell line or stable stem cell culture (e.g. an HSC culture, preferably wherein the HSC is derived from a donor selected according to the method as taught herein) is obtainable (e.g. obtained) by a method of the present invention. Progenitor cells suitable for use in the methods of the invention The methods of second aspect of the invention make use of populations of progenitor cells (preferably granulocyte progenitor cells) as the “starting material” from which granulocytes and / or granulocyte precursors are produced. As noted above, some embodiments of the methods of the invention may also incorporate an optional step of culturing a population of stem cells (e.g. HSCs) to produce a population of granulocyte progenitor cells. Preferably, the methods of the invention incorporate a step of culturing a population of stem cells, preferably a population of HSCs derived from a human donor selected according to the method as taught herein, to produce a population of granulocyte progenitor cells. Preferably, a population of HSCs derived from a donor selected according to the method as taught herein is the “starting material” from which granulocytes and / or granulocyte precursors (preferably granulocyte precursors) are produced. Progenitor cells (preferably granulocyte progenitor cells), and populations of progenitor cells (preferably population of granulocyte progenitor cells), in the context of the present disclosure may usefully be defined by means of their expression of marker profiles and phenotypes. The following definitions, based upon suitable markers expression profiles, may be used singly or in combination to identify suitable populations of progenitor cells (preferably granulocyte progenitor cells). Except for where the context requires otherwise, they should be considered appliable to progenitor cells (preferably granulocyte progenitor cells) as referred to in any embodiment of the invention. A granulocyte progenitor cell may be a cell more differentiated than an HSC but less differentiated than a granulocyte precursor cell. Methods in accordance with the first, second, or third aspects of the invention The first aspect of the invention provides a method of preparing cells (e.g. granulocyte precursor cells) for therapeutic use, the method comprising culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of progenitor cells (e.g. granulocyte progenitor cells), wherein the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) comprise the presence of • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs. The number of cells may increase during this period of cell culture. Accordingly, the period of culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of progenitor cells (e.g. granulocyte progenitor cells) may be referred to as an “expansion phase” or “expansion step”. An expansion phase as described herein may also be used in other methods in accordance with the present invention, such as methods of the third aspect of the invention. The population of stem cells (e.g. HSCs) may be derived from any suitable source of stem cells (preferably a source of stem cells from human origin). Preferably, the population of stem cells (e.g. HSCs) is derived or obtained from a donor, preferably a human donor, having granulocytes (preferably neutrophils) with high cancer killing activity (CKA) (e.g. exhibiting high CKA, e.g. by for instance lysing cancer cells). Granulocytes (preferably neutrophils) may be isolated from peripheral blood of a donor or by leukapheresis using known techniques in the art. Any (in vitro) methods suitable to assess or measure CKA of granulocytes (preferably neutrophils) obtained from a (human) donor may be used. Preferably, the CKA of the granulocytes (preferably neutrophils) is assessed by a method comprising: a) admixing granulocytes (preferably neutrophils) from a donor with cancer cells; b) incubating said admixture; and c) measuring the % of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (preferably neutrophils). The % of cancer cells killed in the admixture in step (c) may be assessed by counting the number of cancer cells left in the admixture at the end of the incubation period (in step b) compared to the number of cancer cells present before admixing the granulocytes (preferably neutrophils) obtained from the (human) donor. For instance, if granulocytes (preferably neutrophils) are added to 100 cancer cells to form an admixture, and 25 cancer cells are left in said admixture at the term of the incubation period (in step b), then the percentage (%) of cancer cells killed is 75%. Alternatively, the following formula may be used to determine the percentage (%) of cancer cells killed. A granulocyte (preferably a neutrophil) with high CKA may be a granulocyte (preferably a neutrophil) having a CKA of at least 30%, for instance at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% or more. Preferably, a granulocyte (preferably a neutrophil) with high CKA is a granulocyte (preferably a neutrophil) having a CKA of at least 30%, preferably at least 50%, more preferably at least 70%. The present inventors have shown that the cancer killing efficacy (or cancer killing activity) of granulocytes (e.g. neutrophils) is genetically-defined, rather than epigenetically-defined. This is demonstrated in e.g., WO2019081879A1, which shows that granulocytes (preferably neutrophils) derived (differentiated in vitro) from HSCs isolated (obtainable or obtained) from a (human) donor have similar cancer killing efficacy (cancer killing activity, e.g. ability to lyse cancer cells) to mature granulocytes isolated (e.g. freshly isolated from blood) directly from the same donor. Advantageously, donors found to have granulocytes (preferably neutrophils) with a high cancer killing activity can be used as a source of HSCs, which can be differentiated (in vitro) into granulocyte precursors with similarly high cancer killing activity. Said granulocyte precursors will, in turn, differentiate into granulocytes (preferably neutrophils) in vitro as well as in vivo over time following administration to an organism (e.g. mice) or a subject (e.g. human subject), and based on the same genetic mechanisms, will exhibit a similarly high cancer killing activity. This is beneficial as such HSCs can advantageously be stored and used for the production of high volumes of granulocyte precursors for use in treating cancer, thus overcoming problems of isolating sufficient quantities of fresh granulocytes (e.g. neutrophils) from a donor, which is a limitation of the current therapeutic methods. The term “obtainable” as used herein also encompasses the term “obtained”. The number of progenitor cells (e.g. granulocyte progenitor cells) may expand by at least 1- fold, at least 2-fold, at least 3-fold, at least 4-fold, at least 5-fold, at least 10-fold, at least 15- fold, at least 20-fold, at least 25-fold, at least 30-fold, at least 35-fold, at least 40-fold, or at least 45-fold as compared to the number of stem cells (e.g. HSCs) present at the start of the cell culture. Indeed, the number of progenitor cells (e.g. granulocyte progenitor cells) may expand by at least 50-fold, at least 100-fold, at least 150-fold, at least 200-fold, at least 250- fold, at least 300-fold, at least 350-fold, at least 400-fold, at least 450-fold, at least 500-fold, at least 550-fold, at least 600-fold, at least 650-fold, at least 700-fold, at least 750-fold, at least 800-fold, at least 850-fold, at least 900-fold, at least 950-fold, at least 1000-fold as compared to the number of stem cells (e.g. HSCs) present at the start of the cell culture. A method in accordance with the first aspect of the invention will employ a basal medium in which cells are cultured. Suitably the basal medium employed in an expansion step in accordance with the invention may be Iscove’s modified Dulbecco’s medium (IMDM). Preferably, the basal medium employed in an expansion step in accordance with the invention may be Iscove’s modified Dulbecco’s medium (IMDM). In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is provided at a concentration within the range of 5nM - 1.5µM. For example, the pyrimido-[4,5-b]-indole derivative may be provided at a concentration within the range of 15nM - 1.5µM. Suitably the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) further comprise: • ITS; and / or • HSA. In a suitable embodiment the cell culture conditions for producing the progenitor cells (e.g. granulocyte precursors) comprise one or more conditions independently selected from the group consisting of: • SCF at a concentration of approximately 0.1-0.2 µg / ml; • FLT-3 ligand at a concentration of approximately 0.1-0.2 µg / ml; • TPO at a concentration of approximately 0.01-0.02 µg / ml; and • HAS at a concentration of approximately 1%. Suitably the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) further comprise: • IL-3; and / or • IL-6. By way of example, the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) may comprise: • IL-3 at a concentration of approximately 0.0001-0.015 µg / ml; and / or • IL-6 at a concentration of approximately 0.0001-0.015 µg / ml. Suitably the pyrimido-[4,5-b]-indole derivative used in the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) is selected from the group consisting of: (1r,4r)-N1-(2-benzyl-7-(2-methyl-2H-tetrazol-5-yl)-9H-pyrimido[4,5-b]indol-4- yl)cyclohexane-1,4-diamine (commonly referred to as UM171), and Methyl 4-((3-(piperidin-1- yl)propyl)amino)-9H-pyrimido[4,5-b] indole-7-carboxylate (commonly referred to as UM729). In a suitable embodiment, the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) may comprise the pyrimido-[4,5-b]-indole derivative UM171 at a concentration within the range of 15nM – 250nM. The cell culture conditions may comprise UM171 at a concentration within the range of 25nM – 100nM. In a suitable embodiment, the cell culture conditions for producing the progenitor cells (e.g. granulocyte progenitor cells) may comprise the pyrimido-[4,5-b]-indole derivative UM729 at a concentration within the range of 250nM – 1.5µM. For example, the cell culture conditions may comprise UM729 at a concentration within the range of 500nM – 1µM. Incidences on which a pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be provided to cells may be separated by up to 5 days, up to 4 days, up to 3 days, up to 2 days, or by a single day. For example, different incidences of providing a pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be separated by approximately 120 hours, by approximately 96 hours, by approximately 72 hours, by approximately 48 hours, or by approximately 24 hours. Suitably, the pyrimido-[4,5-b]-indole derivative is provided to the cells in multiple incidences during the culture to produce the progenitor cells (e.g. granulocyte precursor cells). For example, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be provided to the cells in 1 – 10 incidences during the culture to produce the progenitor cells (e.g. granulocyte precursor cells). Suitably, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be provided to the cells in 4 incidences during the expansion phase. Suitably, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be provided to the cells in 3 incidences during the expansion phase. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) is provided to the cells in a first incidence 24 hours post-seeding. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) is provided to the cells in a second incidence 72 hours after the first incidence. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) is provided to the cells in a third incidence 48 hours after the second incidence. Suitably, the pyrimido-[4,5-b]-indole derivative is provided to the cells at the first incidence one day post-seeding. The pyrimido-[4,5-b]-indole derivative may be provided to the cells at the second incidence four days post-seeding. Suitably, the pyrimido-[4,5-b]-indole derivative is provided to the cells at the third incidence six days post-seeding. In a suitable embodiment the pyrimido-[4,5-b]-indole derivative is provided in the first incidence at a concentration within the range of 15nM - 1.5µM. In such an embodiment employing UM171, UM171 may be provided in the first incidence at a concentration within the range of 25 – 100nM. For example, UM171 may be provided in the first incidence at a concentration of approximately 100nM. In such an embodiment employing UM729, UM729 may be provided in the first incidence at a concentration within the range of 500 nM - 1 µM. For example, UM729 may be provided in the first incidence at a concentration of approximately 500 nM. In a suitable embodiment the pyrimido-[4,5-b]-indole derivative is provided in a second incidence at a concentration within the range of 15nM - 1.5µM. In such an embodiment employing UM171, UM171 may be provided in a second incidence at a concentration within the range of 25 – 100 nM. For example, UM171 may be provided in the second incidence at a concentration of approximately 50 nM. In such an embodiment employing UM729, UM729 may be provided in the second incidence at a concentration within the range of 500 nM - 1 µM. For example, UM729 may be provided in the second incidence at a concentration of approximately 500 nM. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is provided in a third incidence at a concentration within the range of 15nM - 1.5µM. In such an embodiment employing UM171, UM171 may be provided in the third incidence at a concentration within the range of 25 – 100 nM. For example, UM171 may be provided in the third incidence at a concentration of approximately 100 nM. In such an embodiment employing UM729, UM729 may be provided in the third incidence at a concentration within the range of 500 nM - 1 µM. For example, UM729 may be provided in the third incidence at a concentration of approximately 1 µM. Suitably, the concentration of the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) used in the cell culture conditions for producing the progenitor cells (e.g. granulocyte precursor cells) is the same on each incidence of administration. When present, the concentration of the pyrimido-[4,5-b]-indole derivative (such as UM729 or UM171) may be kept substantially constant throughout the cell culture conditions for producing the progenitor cells (e.g. granulocyte precursor cells). A method in accordance with the first aspect of the invention may, further comprise a step of culturing the progenitor cells (e.g. granulocyte precursor cells) to promote their differentiation into granulocytes, or granulocyte precursor cells. Such a step may be in accordance with the second aspect of the invention. The second aspect of the invention provides a (in vitro) method of preparing cells for therapeutic use, the method comprising culturing a population of progenitor cells in cell culture conditions that promote differentiation of the progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursors), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. The cell culture conditions which bring about the differentiation of progenitor cells (e.g. granulocyte precursor cells) to granulocytes, or precursors thereof (preferably granulocyte precursors), used in these methods of the second aspect of the invention, may be referred to as a “differentiation phase” or “differentiation step”. In a suitable embodiment of a method of the second aspect of the invention, the population of progenitor cells (e.g. granulocyte precursor cells) have been produced by a method in accordance with the first aspect of the invention (and optionally in accordance with any of the embodiments of the first aspect of the invention set out herein). Suitably in a population of progenitor cells (e.g. granulocyte precursor cells) produced by a method of the first aspect of the invention, and / or used in a method of the second aspect of the invention: • at least 50% of the cells of the population express CD34; • at least 50% of the cells of the population express CD13; • at least 50% of the cells of the population express HLA-DR; • at least 50% of the cells of the population express CD49d; • at least 50% of the cells of the population express CD33; • less than 50% of the cells of the population express CD15; • less than 50% of the cells of the population express CD38; and / or (preferably and) • less than 50% of the cells of the population express CD45RA. By way of example, in a suitable embodiment of a population of progenitor cells- (e.g. granulocyte precursor cells): • between 70% and 100% of the cells of the population express CD34; and / or • between 80% and 100% of the cells of the population express CD13; and / or • between 70% and 100% of the cells of the population express HLA-DR; and / or • between 80% and 100% of the cells of the population express CD49d; and / or • between 80% and 100% of the cells of the population express CD33; and / or • between 0% and 10% of the cells of the population express CD15; and / or • between 10% and 50% of the cells of the population express CD38; and / or • between 10% and 40% of the cells of the population express CD45RA. Suitably, in a population of progenitor cells (e.g. granulocyte precursor cells): • between 70% and 100% of the cells of the population express CD34; • between 80% and 100% of the cells of the population express CD13; • between 70% and 100% of the cells of the population express HLA-DR; • between 80% and 100% of the cells of the population express CD49d; • between 80% and 100% of the cells of the population express CD33; • between 0% and 10% of the cells of the population express CD15; • between 10% and 50% of the cells of the population express CD38; and / or (preferably and) • between 10% and 40% of the cells of the population express CD45RA. In a suitable embodiment of a method of the second aspect of the invention, each of SCF, TPO, and G-CSF are provided in first and second incidences of administration during the culturing in conditions that promote differentiation of granulocyte progenitors into granulocytes, or precursors thereof (e.g. granulocyte precursors). In such an embodiment, the amount of each of SCF, TPO, and G-CSF provided in the second incidence of administration is approximately double that provided in the first incidence of administration. By way of example, the amount of each of SCF, TPO, and G-CSF provided in the first incidence of administration may be approximately 0.333 ng per 1000 cells. Suitably, the amount of each of SCF, TPO, and G-CSF provided in the second incidence of administration may be approximately 0.666 ng per 1000 cells. In a suitable embodiment of a method of the second aspect of the invention, the first incidence of administration of SCF, TPO, and G-CSF is on the first day of culturing in cell culture conditions that promote differentiation. In a suitable embodiment of a method of the second aspect of the invention, the second incidence of administration of SCF, TPO, and G-CSF is approximately 48 hours after the first incidence. Suitably, the cell culture conditions that promote differentiation of the progenitor cells (e.g. granulocyte precursor cells) into granulocytes, or precursors thereof (e.g. granulocyte precursors), further comprise at least one supplement from the group consisting of: • GM-CSF • IL-3 • TNFa In such an embodiment, the cell culture conditions that promote differentiation of the progenitor cells (e.g. granulocyte precursor cells) into granulocytes, or precursors thereof (e.g. granulocyte precursors), comprise one, two or three of the following: • GM-CSF at a concentration of approximately 0.01 µg / ml; • IL-3 at a concentration of approximately 0.13 µg / ml; and • TNFa at a concentration of approximately 0.001µg / ml. In a suitable embodiment, the cell culture conditions that promote differentiation of the progenitor cells (e.g. granulocyte precursor cells) into granulocytes, or precursors thereof (e.g. granulocyte precursors), comprise each of the following: • GM-CSF at a concentration of approximately 0.01 µg / ml; and • IL-3 at a concentration of approximately 0.13 µg / ml; and • TNFa at a concentration of approximately 0.001µg / ml. Suitably, GM-CSF and IL-3 are provided to the cells for the final 48 hours of the period of culture in conditions that promote differentiation of the progenitor cells (e.g. granulocyte precursor cells) into granulocytes, or precursors thereof (e.g. granulocyte precursors). In contrast, TNFa may suitably be provided to the cells for the final 24 hours of the period of culture in conditions that promote differentiation of the progenitor cells (e.g. granulocyte precursor cells) into granulocytes, or precursors thereof (e.g. granulocyte precursors). The basal medium employed in a differentiation step in accordance with the invention may suitably be Stemline II. In an alternative embodiment, the basal medium employed in a differentiation step in accordance with the invention may suitably be IMDM. Alternatively, in a suitable embodiment, the basal medium is not IMDM. Preferably, the basal medium is not Stemline II. Preferably, the basal medium is IMDM. A method of the second aspect of the invention, or a method employing such a differentiation step (such as a method in accordance with the third aspect of the invention) may achieve an at least 300-fold expansion cell numbers. Indeed, such a method may achieve an at least 450-fold expansion of cell numbers. Such expansions may be achieved in the differentiation phase, or in a combination of an expansion phase (if present) and the differentiation phase. As set out above, the third aspect of the invention provides a (in vitro) method of preparing cells (e.g. granulocytes or precursors thereof, preferably granulocyte precursor cells) for therapeutic use, the method comprising: culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte precursor cells comprise the presence of: • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs; to produce the population of granulocyte progenitor cells, and further comprising culturing granulocyte progenitor cells of this population in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursors), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. It will be appreciated that this third aspect of the invention incorporates features of both the first and second aspects of the invention. Accordingly, the various embodiments previously described in connection with the first and second aspects of the invention should also be taken as disclosed mutatis mutandis as embodiments suitable to be employed in the methods of the third aspect of the invention. Cell culture conditions suitable for use in the methods of the invention The following paragraphs provide guidance as to certain embodiment that may be used in respect of the culture conditions employed in the methods of the invention. Except for where context requires otherwise, these embodiments may be used in methods in accordance with the first aspect of the invention, the second aspect of the invention, or the third aspect of the invention. Suitably, cytokine concentrations provided may be based on the volume of media that is added and is not always a reflection of the concentration of the cytokine overall when in culture. This may be born in mind when considering the volumes of media used to ‘top up’ the culture. Alternatively, in the case of TNFa, the concentration may be based on the total volume of culture as this cytokine is added separately. References to concentrations of pyrimido-[4,5-b]-indole derivatives used may be based on the concentration of the compound overall when in culture. Cell culture conditions suitable for use in expansion steps in accordance with the invention Suitably, the expansion medium may comprise Iscove’s Modified Dulbecco’s Medium (IMDM). Preferably, the expansion medium comprises Iscove’s Modified Dulbecco’s Medium (IMDM). In a suitable embodiment, an expansion step lasts from day E0 to day E8. Preferably the expansion step lasts from day E0 to day E8. Cytokines suitable for use in expansion steps The expansion steps described in the methods of the first aspect of the invention (which may also be used in methods of the third aspect of the invention employ required cytokines, and may further employ optional cytokines, as discussed further below. Required cytokines SCF, FLT3-L and TPO Methods of the invention comprising an expansion step as set out in the second aspect of the invention utilise cell culture condition in which stem cell factor (SCF), FLT-3 ligand (FLT3- L) and thrombopoietic (TPO) are all present. In a suitable embodiment, SCF is provided at a concentration of approximately 0.01-10 µg / ml. Suitably, SCF may be provided at a concentration of approximately 0.05-0.3 µg / ml. For example, SCF may be provided at a concentration of approximately 0.1-0.2 µg / ml. In a suitable embodiment, FLT-3 ligand is provided at a concentration of approximately 0.01- 10 µg / ml. Suitably, FLT-3 ligand may be provided at a concentration of approximately 0.05- 0.3 µg / ml. For example, FLT-3 ligand may be provided at a concentration of approximately 0.1-0.2 µg / ml. In a suitable embodiment, TPO is provided at a concentration of approximately 0.001-0.2 µg / ml. Suitably, TPO may be provided at a concentration of approximately 0.005-0.03 µg / ml. For example, TPO may be provided at a concentration of approximately 0.01-0.02 µg / ml. Optional cytokines IL-3 and IL-6 An expansion phase to be employed in a method of the invention may optionally also comprise supplementation with the cytokines interleukin-3 (IL-3) and / or interleukin-6 (IL-6). Protocols in which supplementation with both IL-3 and IL-6 is employed are referred to at various points in this specification as protocol “v0.4c”. In contrast, protocols which omit supplementation with both IL-3 and IL-6 may be referred to in the specification as protocol “v0.4d”. In the case that supplementation with IL-3 and / or IL-6 is to be used in an expansion step of the invention, IL-3 may be provided in the culture conditions at a concentration of approximately 0.0001-0.015 µg / ml. IL-6 may be provided in the culture conditions at a concentration of approximately 0.0001-0.015 µg / ml. It may be preferred to employ a method of the invention in which the expansion phase is not supplemented with IL-3 or with IL-6 (the “v0.4d” protocol). Other supplements suitable for use in expansion steps Suitably, the expansion medium may comprise insulin-transferrin-selenium (ITS) and / or human serum albumin (HSA). The HSA may be recombinant HSA. Suitably HSA may be provided at a weight / volume (w / v) concentration of approximately 0.1% – 5%. For example, HSA provided as a supplement may be provided at a concentration of approximately 1%. In a suitable embodiment, on the first day of expansion the medium to be used in a method in accordance with the first aspect of the invention comprises IMDM with L-glutamine, 1 X ITS, 1% HSA, SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml), IL-3 (0.015 µg / ml), and IL-6 (0.015 µg / ml). In a suitable embodiment, on the first day of expansion the medium to be used in a method in accordance with the first aspect of the invention comprises IMDM with glutaMAX, 1 X ITS, 1% HSA, SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml), IL-3 (0.015 µg / ml), and IL-6 (0.015 µg / ml). In a suitable embodiment, on the first day of expansion the medium to be used in a method in accordance with the first aspect of the invention comprises IMDM with L-glutamine, 1 X ITS, 1% HSA, SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), and TPO (0.02 µg / ml). In a suitable embodiment, on the first day of expansion the medium to be used in a method in accordance with the first aspect of the comprises IMDM with glutaMAX, 1 X ITS, 1% HSA, SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), and TPO (0.02 µg / ml). Pyrimido-[4,5-b]-indole derivatives suitable for use in the methods of the invention A class of compounds known as pyrimido-[4,5-b]-indole derivatives are known to promote the expansion of hematopoietic stem cells, and to promote the retention of “stemness” in stem cells cultured in their presence. Examples of such compounds include the commercially available agents UM171 and UM729, the structures of which are set out in the Figures. UM171 represents a favoured example of a pyrimido-[4,5-b]-indole derivative that may be used in the methods of the invention. Suitably, the pyrimido-[4,5-b]-indole derivative may be provided to the cells in one incidence, two incidences, three incidences, four incidences, or five incidences during the expansion phase. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is provided to the cells in four incidences during the expansion phase. In such an embodiment the incidences may suitably take place on E0, E4, E6 and E8. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is provided to the cells in three incidences during the expansion phase. In such an embodiment the incidences may suitably take place on E0, E4 and E6. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is UM171, which is provided to the cells during expansion in four incidences. Suitably these incidences are at E0, E4, E6 and E8. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is UM171, which is provided to the cells during expansion in three incidences. Suitably, the pyrimido-[4,5-b]-indole derivative is UM171, which is provided to the cells during expansion in three incidences at E0, E4, and E6. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is UM171, which is provided to the cells during expansion in three incidences at E1, E4, and E6. For example, the UM171 may be provided to the cells at a concentration of 50 nM at E1, at a concentration of 25 nM at E4, and at a concentration of 50 nM at E6. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is UM729, which is provided to the cells during expansion in three incidences at E0, E4, and E6. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative is UM729 and is provided to the cells during expansion in three incidences at E1, E4, and E6. In a suitable example, the UM729 may be provided to the cells at a concentration of 500 nM at E1, at a concentration of 50 nM at E4, and at a concentration of 1µM at E6. Suitably, the pyrimido-[4,5-b]-indole derivative may be provided at a concentration within the range of 15 nM – 1.5µM. In a suitable embodiment, the pyrimido-[4,5-b]-indole derivative (such as UM171 or UM729) may be provided at a concentration of approximately 50nM – 1µM. For example, the pyrimido-[4,5-b]-indole derivative may be provided at a concentration of approximately 50 nM, approximately 100 nM, approximately 150 nM, approximately 200 nM, approximately 250 nM, approximately 300 nM, approximately 350 nM, approximately 400 nM, approximately 450 nM, approximately 500 nM, approximately 550 nM, approximately 600 nM, approximately 650 nM, approximately 700 nM, approximately 750 nM, approximately 800 nM, approximately 850 nM, approximately 900 nM, approximately 950 nM, approximately 1 µM, approximately 1.25 µM, approximately 1.5 µM. Optionally, the cell culture conditions may further comprise: ITS; and / or HSA. Similarly, the cell culture conditions may comprise one or more conditions independently selected from the group consisting of: SCF at a concentration of approximately 0.2 µg / ml; FLT-3 ligand at a concentration of approximately 0.2 µg / ml; TPO at a concentration of approximately 0.2 µg / ml; and HSA at a concentration of approximately 1%. Differentiation conditions suitable for use in the methods of the invention Methods of the invention (for example methods in accordance with the second or third aspect of the invention) may comprise a differentiation step, in which cells are culture in conditions the promote differentiation of a population of progenitor cells (e.g. granulocyte progenitor cells) into a population of granulocytes, or precursors thereof (e.g. granulocyte precursors). Suitably the cells produced may be neutrophils (or precursors thereof). Preferably, the cells produced by the methods of the invention are granulocytes precursor cells. The granulocyte precursor cells may be: common myeloid progenitor cells, granulocyte monocyte progenitor cells, myeloblasts, promyelocytes, myelocytes, metamyelocytes, band cells, or any intermediate cells thereof or cells equivalent thereto. More preferably, the granulocyte precursor cells are promyelocytes, myelocytes or cells that are an intermediate thereof. Yet more preferably, the granulocyte precursor cells are promyelocytes, myelocytes, or cells that are intermediate thereof or any combination thereof. Cells described herein are preferably human cells (e.g. derived from human cells). In a suitable embodiment, a differentiation step lasts from day D0 to day D4. In a method comprising an expansion step in accordance with the first aspect of the invention, E8 of the expansion step may correspond to D0 of the differentiation step. Cell culture conditions suitable for use in expansion steps in accordance with the invention Cell culture conditions suitable for use in differentiation steps in accordance with the invention The basal medium employed in a differentiation step in accordance with the invention may suitably be Stemline II. Preferably, the basal medium employed in a differentiation step in accordance with the invention is not stem line II. In an alternative embodiment, the basal medium employed in a differentiation step in accordance with the invention may suitably be IMDM. Alternatively, in a suitable embodiment, the basal medium is not IMDM. Preferably, the basal medium employed in a differentiation step in accordance with the invention is IMDM. Cytokines for use in differentiation steps In a suitable embodiment of a differentiation step (for example, in a method of the second aspect of the invention) one, two or three of each of SCF, TPO, and G-CSF provided in a first incidence of administration may be provided in an amount of between approximately 0.111 ng and 0.555 ng per 1000 cells, for example an amount of between approximately 0.222 ng and 0.444 ng per 1000 cells, such as approximately 0.333 ng per 1000 cells in culture. In a suitable embodiment of a differentiation step (for example, in a method of the second aspect of the invention) one, two or three of each of SCF, TPO, and G-CSF provided in a second incidence of administration may be provided in an amount approximately twice that provided in the first incidence of administration. For example, one, two or three of each of SCF, TPO, and G-CSF provided in a second incidence of administration may be provided in an amount of between approximately 0.444 ng and 0.888 ng per 1000 cells, for example an amount of between approximately 0.555 ng and 0.777 ng per 1000 cells, such as approximately 0.666 ng per 1000 cells in culture. A differentiation step suitable for use in the methods of the invention will also utilise cell culture conditions that comprise supplementation with one, two or three cytokines selected from the group consisting of: granulocyte-macrophage colony-stimulation factor (GM-CSF), interleukin-3 (IL-3) and tumour necrosis factor alpha (TNFa). For example, a differentiation step suitable for use in the methods of the invention will make use of cell culture conditions that comprise one, two or three of the following: • GM-CSF at a concentration of approximately 0.001 - 0.03 µg / ml; • IL-3 at a concentration of approximately 0.05 - 0.2 µg / ml; and • TNFa at a concentration of approximately 0.0001 - 0.005 µg / ml. Suitably, a differentiation step suitable for use in the methods of the invention makes use of cell culture conditions that comprise one, two or three of the following: • GM-CSF at a concentration of approximately 0.01 µg / ml; • IL-3 at a concentration of approximately 0.13 µg / ml; and • TNFa at a concentration of approximately 0.001µg / ml. In a suitable embodiment, cell culture conditions used in a differentiation step employed in a method of the invention comprise each of the following: • GM-CSF at a concentration of approximately 0.01 µg / ml; and • IL-3 at a concentration of approximately 0.13 µg / ml; and • TNFa at a concentration of approximately 0.001µg / ml. In one aspect, the invention relates to a method of preparing cells (e.g. granulocyte precursor cells) for therapeutic use, the method comprising culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte progenitor cells comprise the presence of: (i) SCF; (ii) FLT-3 ligand; (iii) TPO; and (iv) a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSC. Preferably, the population of stem cells has been derived from a donor having granulocytes (preferably neutrophils) with high CKA. Preferably, the CKA is assessed by a method comprising: a) admixing granulocytes (preferably neutrophils) from a donor with cancer cells; b) incubating said admixture; and c) measuring the % of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (preferably neutrophils). Preferably, the granulocytes (preferably neutrophils) have a CKA of at least 30%, preferably at least 50%, more preferably at least 70%. Preferably, the pyrimido-[4,5-b]-indole derivative is provided at a concentration within the range of 15nM - 1.5µM. Preferably, the pyrimido-[4,5-b]-indole derivative is one of: UM171 or UM729, preferably UM171. Preferably, the cell culture conditions further comprise: ITS; and / or HSA. Preferably, the cell culture conditions comprise one or more conditions independently selected from the group consisting of: SCF at a concentration of approximately 0.1-0.2 µg / ml; FLT-3 ligand at a concentration of approximately 0.1-0.2 µg / ml; TPO at a concentration of approximately 0.01-0.02 µg / ml; and HSA at a concentration of approximately 1%. Preferably, the cell culture conditions comprise (e.g. further comprise): IL-3 at a concentration of approximately 0.0001-0.015 µg / ml; and / or IL-6 at a concentration of approximately 0.0001-0.015 µg / ml. In one aspect, the invention provides a method of preparing cells (e.g. granulocytes or granulocyte precursors, preferably granulocyte precursor cells) for therapeutic use, the method comprising culturing a population of granulocyte progenitor cells in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or granulocyte precursors (preferably granulocyte precursor cells), the cell culture conditions comprising the presence of: (i) a basal medium; (ii) SCF; (iii) TPO; and (iv) G-CSF. Preferably, the population of granulocyte progenitor cells have been produced by the method as taught herein. Preferably, each of SCF, TPO, and G-CSF are provided in first and second incidences of administration during the culturing in conditions that promote differentiation into granulocytes, or precursors thereof (preferably granulocyte precursor cells). Preferably, the amount of each of SCF, TPO, and G-CSF provided in the second incidence of administration is approximately double that provided in the first incidence of administration (preferably is double that provided in the first incidence of administration). Preferably, the amount of each of SCF, TPO, and G-CSF provided in the first incidence of administration is approximately 0.333 ng per 1000 cells (preferably is 0.333 ng per 1000 cells). Preferably, the concentration of each of SCF, TPO, and G-CSF provided in the second incidence of administration is approximately 0.666 ng per 1000 cells (preferably is 0.666 ng per 1000 cells). Preferably, the cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells), further comprise: GM-CSF at a concentration of approximately 0.01 µg / ml; and IL-3 at a concentration of approximately 0.13 µg / ml; and TNFa at a concentration of approximately 0.001µg / ml. Preferably, GM-CSF and IL-3 are provided to the cells (preferably granulocyte precursor cells) for the final 48 hours of a period of culture in conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells). Preferably, TNFa is provided to the cells (preferably granulocyte precursor cells) for the final 24 hours of a period of culture in conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells). In one aspect, the invention provides a method of preparing cells (e.g. granulocytes, or precursors thereof, preferably granulocyte precursor cells) for therapeutic use, the method comprising: culturing a population of stem cells (preferably HCSs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte precursor cells comprise the presence of: • SCF; • FLT-3 ligand; • TPO; and • a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs; to produce the population of granulocyte progenitor cells; and further comprising culturing the granulocyte progenitor cells of said population in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells), the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. Preferably, the method further comprises recovering the granulocytes, or precursors thereof (preferably granulocyte precursor cells). Preferably, the method further comprises cryopreserving the granulocytes, or precursors thereof (preferably granulocyte precursor cells). Preferably, the method is devoid of animal-derived products. Preferably, the stem cell is an HSC, preferably a human HSC. Preferably, the granulocyte precursor cell is a promyelocyte, a myelocyte, or an intermediate thereof. Exemplary populations of progenitor cells (e.g. granulocyte precursor cells) The methods of the first aspect of the invention result in the production of populations of progenitor cells (e.g. granulocyte precursor cells). Populations of progenitor cells (e.g. granulocyte precursor cells) are also employed in the methods of the second aspect of the invention, in which they differentiate to produce populations of granulocytes, or precursors thereof (e.g. granulocyte precursors). In a suitable embodiment of a population of progenitor cells (e.g. granulocyte precursor cells): • at least 50% of the cells of the population express CD34; • at least 50% of the cells of the population express CD13; • at least 50% of the cells of the population express HLA-DR; • at least 50% of the cells of the population express CD49d; • at least 50% of the cells of the population express CD33; • less than 50% of the cells of the population express CD15; • less than 50% of the cells of the population express CD38; and / or (preferably and) • less than 50% of the cells of the population express CD45RA. By way of example, in a suitable embodiment of a population of progenitor cells (e.g. granulocyte precursor cells): • between 80% and 90% of the cells of the population express CD34; and / or • between 90% and 100% of the cells of the population express CD13; and / or • between 70% and 85% of the cells of the population express HLA-DR; and / or • between 95% and 100% of the cells of the population express CD49d; and / or • between 95% and 10% of the cells of the population express CD33; and / or • between 0% and 10% of the cells of the population express CD15; and / or • between 20% and 50% of the cells of the population express CD38; and / or • between 15% and 30% of the cells of the population express CD45RA. Suitably, in a population of progenitor cells (e.g. granulocyte precursor cells): • between 80% and 90% of the cells of the population express CD34; • between 90% and 100% of the cells of the population express CD13; • between 70% and 85% of the cells of the population express HLA-DR; • between 95% and 100% of the cells of the population express CD49d; • between 95% and 10% of the cells of the population express CD33; • between 0% and 10% of the cells of the population express CD15; • between 20% and 50% of the cells of the population express CD38; and • between 15% and 30% of the cells of the population express CD45RA. Populations of cells of the invention (granulocytes, or precursors thereof, and neutrophils, or precursors thereof) The term “granulocyte” as used herein may refer to a class of white blood cells characterized by the presence of one or more granules in their cytoplasm. A granulocyte may be a neutrophil, eosinophil, or basophils. Preferably, the granulocyte is a neutrophil. The term “granulocyte precursor” (e.g. as used in the context of “granulocyte or precursor thereof”) refers to a cell that is capable of differentiating into a granulocyte. A granulocyte precursor may be any granulocyte precursor downstream from an HSC. A granulocyte precursor may be a common myeloid progenitor cell, a granulocyte monocyte progenitor cell, a myeloblast, a promyelocyte, a myelocyte, a metamyelocyte, a band cell, or any intermediate cell thereof or a cell equivalent thereto. Preferably, a granulocyte precursor may be a promyelocyte, a myelocyte, or an intermediate thereof, more preferably an intermediate thereof. An intermediate may exhibit one or more characteristics of the two types of cells described herein to which it is the intermediate. The granulocytes precursor may be a population of cells comprising a plurality of a single granulocyte precursor type, e.g. a population of cells comprising a plurality of myeloblasts or it may be a population of cells comprising a mixture of different granulocytes precursor types, e.g. a population of cells comprising a mixture of common myeloid progenitor cells, granulocyte monocyte progenitor cells, myeloblasts, promyelocytes, myelocytes, metamyelocytes, band cells, and / or any intermediate cells. More preferably, the granulocyte precursors may be a population of cells comprising a plurality of a single granulocyte precursor type, e.g. a population of cells comprising a plurality of myeloblasts or a population of promyelocytes or a population of myelocytes or a population of cells that are an intermediate between a promyelocyte and a myelocyte or it may be a population of cells comprising a mixture (e.g. combination) of different granulocytes precursor types, e.g. a population of cells comprising a mixture (e.g. combination) of promyelocytes and myelocytes or a population of cells comprising a mixture of common myeloid progenitor cells, granulocyte monocyte progenitor cells, myeloblasts, promyelocytes, myelocytes, metamyelocytes, band cells, and / or any intermediate cells. Preferably, the granulocyte precursor cell is a promyelocyte, a myelocyte, or a cell that is an intermediate thereof. More preferably, the granulocyte precursor is a combination of promyelocytes, myelocytes, and cells that are intermediate thereof. Preferably, a granulocyte precursor may be committed to becoming a granulocyte. A granulocyte precursor is preferably committed to becoming a granulocyte, such as a neutrophil, in vitro, in vivo or ex vivo. A granulocyte or precursor thereof according to the present invention may not necessarily be identical to a granulocyte or precursor thereof found in vivo (e.g. in a human). The granulocyte or precursor thereof may have one or more characteristics in common with a corresponding granulocyte or precursor thereof found in vivo (e.g. in a human). The granulocyte or precursor thereof may have one or more characteristics that are different to a corresponding granulocyte or precursor thereof found in vivo (e.g. in a human). Preferably, the granulocyte or precursor thereof may have one or more characteristics in common and one or more characteristics that are different to a corresponding granulocyte or precursor thereof found in vivo (e.g. in a human). A granulocyte or precursor thereof is preferably one that has been differentiated in vitro. The granulocyte or precursor thereof may have one or more characteristics in common with a corresponding granulocyte or precursor thereof produced by a different in vitro method. The granulocyte or precursor thereof may have one or more characteristics that are different to a corresponding granulocyte or precursor thereof produced by a different in vitro method. Preferably, the granulocyte or precursor thereof may have one or more characteristics in common and one or more characteristics that are different to a corresponding granulocyte or precursor thereof produced by a different in vitro method. The granulocyte or precursor thereof is preferably an equivalent granulocyte or precursor thereof. Said one or more characteristics may include one or more of: morphology; cell surface markers; a gene expression profile; cancer killing activity; immunomodulatory properties; persistence; viability; and / or longevity. Preferably, a granulocyte or precursor thereof (preferably an in vitro differentiated granulocyte precursor cell) according to the present invention is not identical to an in vivo differentiated natural (wild type) granulocyte or precursor thereof, preferably an in vivo differentiated granulocyte precursor of an equivalent developmental stage, found in vivo (e.g. in a human). As exemplified in the examples section, the in vitro differentiated granulocyte precursor cells of the invention may exhibit several distinctive characteristics (e.g. functional and structural), which are not found in granulocyte precursor cells of an equivalent developmental stage that have been differentiated in vivo (e.g. in humans). Without wishing to be bound by theory, it is believed that these unique characteristics, associated with the benefits disclosed herein, are imparted, at least in part, both by the source the start material (HSCs obtained from donors with granulocytes (preferably neutrophils) with high CKA as taught herein via genetically based mechanisms) and by the methods and culture media of the invention. The skilled person understands that, when comparing cells, it is important to identify or determine which “comparator” cells to use for the comparison. The skilled person knows that the comparator cell is preferably a cell at a similar or closely matching point in development, and which is derived from the same organism (e.g. human), so that any differences such as a difference in gene expression, cell surface marker expression, cancer killing activity, immunomodulatory activity or other phenotypes reflect true biological differences (e.g. differences attributed to the methods and media of the invention) rather than artifacts such as developmental timing mismatches, organism mismatches, or biases such as artificial genetic manipulations, exposure to compounds, etc. The term “equivalent” as used in the context of a granulocyte or granulocyte precursor herein may mean a cell that is from the same organism and / or at an equivalent (preferably identical) developmental stage. Preferably, an equivalent granulocyte or granulocyte precursor is a cell that is from the same organism and at an equivalent (preferably identical) developmental stage. For example, when a human granulocyte precursor cell of the invention that has been differentiated in vitro is an intermediate between a promyelocyte and a myelocyte, an equivalent granulocyte precursor cell that has been differentiated in vivo is preferably a human granulocyte precursor cell is an intermediate between a promyelocyte and a myelocyte that has been differentiated in vivo. Preferably, conversely, a neutrophil isolated from peripheral blood is not equivalent to a granulocyte precursor cell of the invention. It is preferred that an equivalent cell has not been genetically engineered and / or exposed to one or more compounds that are not normally found in vivo. The person skilled in the art knows how to determine if two cells are of an equivalent developmental stage. Techniques are known in the art to assign a cell to a particular developmental stage. Such cells may share one or more of characteristics known to be associated with a cell of a particular developmental stage (e.g. in vivo). Said one or more characteristics preferably distinguish said cell from a cell of a different developmental stage. Such characteristics may be one or more of: morphology; cell surface markers; a gene expression profile; cancer killing activity; immunomodulatory properties; persistence; viability; and / or longevity. Preferably, an equivalent developmental stage is the same developmental stage. As set out in the fourth aspect of the invention, cells of the invention may comprise a population of granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: • at least 50% of the cells of the population express CD11b, • at least 50% of the cells of the population express CD15, • at least 50% of the cells of the population express CD64, • at least 50% of the cells of the population express CD89, • at least 50% of the cells of the population express CXCR2, • at least 50% of the cells of the population express neutrophil elastase, • less than 50% of the cells of the population express CD14, • less than 50% of the cells of the population express CD19, • less than 50% of the cells of the population express CD3, • less than 50% of the cells of the population express CD34, • less than 50% of the cells of the population express CD66b, • less than 50% of the cells of the population express CD68, • less than 50% of the cells of the population express CXCR4, and / or(preferably and) • less than 50% of the cells of the population express HLA-DR. Suitably, such populations of cells of the invention may be prepared by methods of the invention. A suitable embodiment of the fourth aspect of the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: • between 55% and 65% of the cells of the population express CD11b, and / or • between 70% and 90% of the cells of the population express CD15, and / or • between 70% and 90% of the cells of the population express CD64, and / or • between 75% and 95% of the cells of the population express CD89, and / or • between 50% and 70% of the cells of the population express CXCR2, and / or • between 60% and 80% of the cells of the population express neutrophil elastase, and / or • between 0% and 10% of the cells of the population express CD14, and / or • between 0% and 2.5% of the cells of the population express CD19, and / or • between 0% and 2.5% of the cells of the population express CD3, and / or • between 0% and 10% of the cells of the population express CD34, and / or • between 0% and 20% of the cells of the population express CD66b, and / or • between 0% and 2.5% of the cells of the population express CD68, and / or • between 20% and 40% of the cells of the population express CXCR4, and / or • between 20% and 40% of the cells of the population express HLA-DR. A further suitable embodiment of the fourth aspect of the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: • between 55% and 65% of the cells of the population express CD11b, • between 70% and 90% of the cells of the population express CD15, • between 70% and 90% of the cells of the population express CD64, • between 75% and 95% of the cells of the population express CD89, • between 50% and 70% of the cells of the population express CXCR2, • between 60% and 80% of the cells of the population express neutrophil elastase, • between 0% and 10% of the cells of the population express CD14, • between 0% and 2.5% of the cells of the population express CD19, • between 0% and 2.5% of the cells of the population express CD3, • between 0% and 10% of the cells of the population express CD34, • between 0% and 20% of the cells of the population express CD66b, • between 0% and 2.5% of the cells of the population express CD68, • between 20% and 40% of the cells of the population express CXCR4, and • between 20% and 40% of the cells of the population express HLA-DR. As set out in the fifth aspect of the invention, cells of the invention may comprise a population of granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: • at least 50% of the cells of the population express CD64; and / or • at least 50% of the cells of the population express CD89; and / or neutrophil elastase. As set out in the sixth aspect of the invention, cells of the invention may comprise a population of granulocytes, or precursors thereof, (e.g. granulocyte precursor) wherein: • at least 50% of the cells of the population express CD64; • at least 50% of the cells of the population express CD89; and / or (preferably and) • at least 50% of the cells of the population express neutrophil elastase. In accordance with the seventh aspect, cells of the invention may comprise a population of neutrophils, or precursors thereof (preferably granulocyte precursor cells), expressing neutrophil elastase, and wherein at least 50% of the cells of the population express CD64; and / or CD89. In one aspect, the invention provides a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) obtainable by the methods as taught herein. In one aspect, the invention provides a granulocyte, or granulocyte precursor (preferably granulocyte precursor cell). In one aspect, the invention provides a granulocyte, or precursor thereof obtainable by the methods as taught herein, wherein the granulocyte or granulocyte precursor is a granulocyte precursor cell comprising: a) increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or (preferably and) b) decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one aspect, the invention provides a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) obtainable (or obtained) by a method of the invention, wherein: (i) between 55% and 65% of the cells of the population express CD11b, (ii) between 70% and 90% of the cells of the population express CD15, (iii) between 70% and 90% of the cells of the population express CD64, (iv) between 75% and 95% of the cells of the population express CD89, (v) between 50% and 70% of the cells of the population express CXCR2, (vi) between 60% and 80% of the cells of the population express neutrophil elastase, (vii) between 0% and 10% of the cells of the population express CD14, (viii) between 0% and 2.5% of the cells of the population express CD19, (ix) between 0% and 2.5% of the cells of the population express CD3, (x) between 0% and 10% of the cells of the population express CD34, (xi) between 0% and 20% of the cells of the population express CD66b, (xii) between 0% and 2.5% of the cells of the population express CD68, (xiii) between 20% and 40% of the cells of the population express CXCR4, and / or (preferably and) (xiv) between 20% and 40% of the cells of the population express HLA-DR. In one aspect, the invention provides a population of granulocytes, or precursors thereof (preferably granulocyte precursor cells) as taught herein, comprising granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: (i) at least 50% of the cells of the population express CD64; and / or (preferably and) (ii) at least 50% of the cells of the population express CD89; and / or neutrophil elastase. In one aspect, the invention provides a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) as taught herein, comprising granulocytes, or granulocyte precursors (preferably granulocyte precursor cells), wherein: (i) at least 50% of the cells of the population express CD64; (ii) at least 50% of the cells of the population express CD89; and / or (preferably and) (iii) at least 50% of the cells of the population express neutrophil elastase. Expression of markers within cell populations of the invention The fourth, fifth, sixth and seventh aspects of the invention each relate to a population of cells defined with reference to the markers expressed by the cells, or by particular proportions of the cells. The following paragraphs provide more details of particular embodiments of these aspects. Each of the markers set out in the fourth aspect of the invention is referred to below. It will be appreciated that not all such references are relevant in the case of the populations of cells of the fifth, sixth and seventh aspects of the invention. Embodiments of these aspects of the invention may be further defined with reference to the provisions set out in the following paragraphs in respect of the markers CD64, CD89 and neutrophil elastase (as appropriate). In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD11b. Suitably, at least 50% of a population of cells of the invention express CD11b. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, or at least 95% of the cells of a population of cells of the invention may express CD11b. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90%, approximately 50 to 85%, approximately 50 to 80%, approximately 50 to 75%, or approximately 50 to 70% of the cells of a population of cells of the invention may express CD11b. Suitably, approximately 50 to 65%, approximately 50 to 60%, approximately 50 to 55% of a population of cells of the invention may express CD11b. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100% of the cells of a population of cells of the invention may express CD11b. Suitably, approximately 55 to 95%, approximately 55 to 100%, approximately 55 to 90%, approximately 55 to 85%, approximately 55 to 80%, approximately 55 to 75%, approximately 55 to 70%, approximately 55 to 65% of the cells of a population of cells of the invention may express CD11b. Suitably, approximately 60 to 95%, approximately 60 to 90%, approximately 60 to 85%, approximately 60 to 80%, approximately 60 to 75%, approximately 60 to 70%, approximately 60 to 65% of the cells of a population of cells of the invention may express CD11b. Suitably, approximately 65 to 95%, approximately 65 to 90%, approximately 65 to 85%, approximately 65 to 80%, approximately 65 to 75%, approximately 65 to 70% of the cells of a population of cells of the invention may express CD11b. In a suitable embodiment, 55 to 65% of the cells of a population of cells of the invention may express CD11b. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD15. Suitably, at least 50% of the cells of a population of cells of the invention may express CD15. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% of the cells of a population of cells of the invention may express CD15. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90%, approximately 50 to 85%, approximately 50 to 80% of the cells of a population of cells of the invention may express CD15. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100%, approximately 75 to 100%, approximately 80 to 100%, approximately 85 to 100% of the cells of a population of cells of the invention may express CD15. Suitably, approximately 70 to 95%, approximately 70 to 90%, approximately 70 to 85%, approximately 70 to 80%, approximately 70 to 75% of the cells of a population of cells of the invention may express CD15. Suitably, approximately 75 to 95%, approximately 75 to 90%, approximately 75 to 85%, approximately 75 to 80%, of the cells of a population of cells of the invention may express CD15. Suitably, approximately 80 to 95%, approximately 80 to 90%, approximately 80 to 85% of the cells of a population of cells of the invention may express CD15. In a suitable embodiment, 70 to 90% of the cells of a population of cells of the invention may express CD15. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD64. Suitably, at least 50% of the cells of a population of cells of the invention may express CD64. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% of the cells of a population of cells of the invention may express CD64. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90%, approximately 50 to 85%, approximately 50 to 80% of the cells of a population of cells of the invention may express CD64. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100%, approximately 75 to 100%, approximately 80 to 100%, approximately 85 to 100% of the cells of a population of cells of the invention may express CD64. Suitably, approximately 70 to 95%, approximately 70 to 90%, approximately 70 to 85%, approximately 70 to 80%, approximately 70 –75% of the cells of a population of cells of the invention may express CD64. Suitably, approximately 75 to 95%, approximately 75 to 90%, approximately 75 to 85%, approximately 75 to 80%, of the cells of a population of cells of the invention may express CD64. Suitably, approximately 80 to 95%, approximately 80 to 90%, approximately 80 to 85% of the cells of a population of cells of the invention may express CD64. In a suitable embodiment, 70-90% of the cells of a population of cells of the invention may express CD64. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD89. Suitably, at least 50% of the cells of a population of cells of the invention may express CD89. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% of the cells of a population of cells of the invention may express CD89. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90% of the cells of a population of cells of the invention may express CD89. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100%, approximately 75 to 100%, approximately 80 to 100%, approximately 85 to 100%, approximately 90 to 100% of the cells of a population of cells of the invention may express CD89. Suitably, approximately 70 to 95%, approximately 75 to 95%, approximately 70 to 85%, approximately 75 to 85%, approximately 75 –80% of the cells of a population of cells of the invention may express CD89. Suitably, approximately 80 to 95%, approximately 85 to 95%, approximately 90 to 95%, approximately 80 to 90%, approximately 80 to 85%, approximately 85 to 90% of the cells of a population of cells of the invention may express CD89. In a suitable embodiment, 75-95% of the cells of a population of cells of the invention may express CD89. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CXCR2. Suitably, at least 50% of the cells of a population of cells of the invention may express CXCR2. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% of the cells of a population of cells of the invention may express CXCR2. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90%, approximately 50 to 85%, approximately 50 to 80%, approximately 50 to 75%, approximately 50 to 70%, approximately 50 to 65%, approximately 50 to 60%, approximately 50 to 55% of the cells of a population of cells of the invention may express CXCR2. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100%, approximately 75 to 100% of the cells of a population of cells of the invention may express CXCR2. Suitably, approximately 55 to 95%, approximately 55 to 90%, approximately 55 to 85%, approximately 55 to 80%, approximately 55 –75%, approximately 55 to 70%, approximately 55 to 65%, approximately 55 to 60% of the cells of a population of cells of the invention may express CXCR2. Suitably, approximately 60 to 95%, approximately 60 to 90%, approximately 60 to 85%, approximately 60 to 80%, approximately 60 to 75%, approximately 60 to 70%, approximately 60 to 65%, approximately 65 to 70% of the cells of a population of cells of the invention may express CXCR2. In a suitable embodiment, 50-70% of the cells of a population of cells of the invention may express CXCR2. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of neutrophil elastase. Suitably, at least 50% of the cells of a population of cells of the invention may express neutrophil elastase. Suitably, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% of the cells of a population of cells of the invention may express neutrophil elastase. Suitably, approximately 50 to 100%, approximately 50 to 95%, approximately 50 to 90%, approximately 50 to 85%, approximately 50 to 80%, approximately 50 to 75%, approximately 50 to 70%, approximately 50 to 65%, approximately 50 to 60% of the cells of a population of cells of the invention may express neutrophil elastase. Suitably, approximately 55 to 100%, approximately 60 to 100%, approximately 65 to 100%, approximately 70 to 100%, approximately 75 to 100%, approximately 80 to 100% of the cells of a population of cells of the invention may express neutrophil elastase. Suitably, approximately 55 to 95%, approximately 55 to 90%, approximately 55 to 85%, approximately 55 to 80%, approximately 55 –75%, approximately 55 to 70%, approximately 55 to 65%, approximately 55 to 60% of the cells of a population of cells of the invention may express neutrophil elastase. Suitably, approximately 60 to 95%, approximately 65 to 95%, approximately 60 to 90%, approximately 65 to 90%, approximately 60 to 85%, approximately 65 to 85%, approximately 60 to 80%, approximately 65 to 80%, approximately 60 to 75%, approximately 65 to 70%, approximately 60 to 70%, approximately 60 to 65%, approximately 65 to 70%, approximately 70 to 80% of the cells of a population of cells of the invention may express neutrophil elastase. In a suitable embodiment, 60 to 80% of the cells of a population of cells of the invention may express neutrophil elastase. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD14. Suitably, less than 50% of the cells of a population of cells of the invention may express CD14. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD14. Suitably, approximately 0 to 2.5%, approximately 0 to 5%, approximately 0 to 7.5%, approximately 0 to 10%, approximately 0 to 12.5%, approximately 0 to 15% of the cells of a population of cells of the invention may express CD14. Suitably, approximately 2.5% - 10%, approximately 5% - 10%, approximately 7.5 to 10% of the cells of a population of cells of the invention may express CD14. In a suitable embodiment, 0 to 10% of the cells of a population of cells of the invention may express CD14. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD19. Suitably, less than 50% of the cells of a population of cells of the invention may express CD19. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD19. Suitably, approximately 0 to 1.25%, approximately 0 - 2.5%, approximately 0 to 5%, approximately 1.25 to 2.5% of the cells of a population of cells of the invention may express CD19. In a suitable embodiment, 0 to 2.5% of the cells of a population of cells of the invention may express CD19. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD3. Suitably, less than 50% of the cells of a population of cells of the invention may express CD3. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD3. Suitably, approximately 0 to 1.25%, approximately 0 - 2.5%, approximately 0 to 5%, approximately 1.25 to 2.5% of the cells of a population of cells of the invention may express CD3. In a suitable embodiment, 0 to 2.5% of the cells of a population of cells of the invention may express CD3. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD34. Suitably, less than 50% of the cells of a population of cells of the invention may express CD34. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD34. Suitably, approximately 0 to 2.5%, approximately 0 to 5%, approximately 0 to 7.5%, approximately 0 to 10%, approximately 0 to 12.5%, approximately 0 to 15% of the cells of a population of cells of the invention may express CD34. Suitably, approximately 2.5% - 10%, approximately 5% - 10%, approximately 7.5 to 10% of the cells of a population of cells of the invention may express CD34. In a suitable embodiment, 0 to 10% of the cells of a population of cells of the invention may express CD34. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD56. Suitably, less than 50% of the cells of a population of cells of the invention may express CD56. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD56. Suitably, approximately 0 to 1.25%, approximately 0 - 2.5%, approximately 0 to 5%, approximately 1.25 to 2.5% of the cells of a population of cells of the invention may express CD56. In a suitable embodiment, 0 to 2.5% of the cells of a population of cells of the invention may express CD56. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD66b. Suitably, less than 50% of the cells of a population of cells of the invention may express CD66b. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD66b. Suitably, approximately 0 to 5%, approximately 0 to 10%, approximately 0 to 15%, approximately 0 to 20%, approximately 0 to 25%, approximately 0 to 30% of the cells of a population of cells of the invention may express CD66b. Suitably, approximately 5% - 10%, approximately 5 to 15%, approximately 5 to 20%, approximately 10 to 15%, approximately 15 to 20% of the cells of a population of cells of the invention may express CD66b. In a suitable embodiment, 0 to 20% of the cells of a population of cells of the invention may express CD66b. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CD68. Suitably, less than 50% of the cells of a population of cells of the invention may express CD68. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CD68. Suitably, approximately 0 to 1.25%, approximately 0 - 2.5%, approximately 0 to 5%, approximately 1.25 to 2.5% of the cells of a population of cells of the invention may express CD68. In a suitable embodiment, 0 to 2.5% of the cells of a population of cells of the invention may express CD68. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of CXCR4. Suitably, less than 50% of the cells of a population of cells of the invention may express CXCR4. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express CXCR4. Suitably, approximately 15 to 50%, approximately 15 to 45%, approximately 15 to 40%, approximately 15 to 35%, approximately 15 to 30%, approximately 15 to 25%, approximately 15 to 20% of the cells of a population of cells of the invention may express CXCR4. Suitably, approximately 20 to 50%, approximately 20 to 45%, approximately 20 to 40%, approximately 20 to 35%, approximately 20 to 30%, approximately 20 to 25% of the cells of a population of cells of the invention may express CXCR4. Suitably, approximately 25 to 50%, approximately 25 to 45%, approximately 25 to 40%, approximately 25 to 35%, approximately 25 to 30% of the cells of a population of cells of the invention may express CXCR4. In a suitable embodiment, 20 to 40% of the cells of a population of cells of the invention may express CXCR4. In certain aspects or embodiments of the invention, a population of cells of the invention may be characterised with respect to their expression of HLA-DR. Suitably, less than 50% of the cells of a population of cells of the invention may express HLA-DR. Suitably, less than 50%, less than 45%, less than 40%, less than 35%, less than 30%, less than 25%, less than 20%, less than 15%, less than 10%, less than 5%, less than 2.5% of the cells of a population of cells of the invention may express HLA-DR. Suitably, approximately 15 to 50%, approximately 15 to 45%, approximately 15 to 40%, approximately 15 to 35%, approximately 15 to 30%, approximately 15 to 25%, approximately 15 to 20% of the cells of a population of cells of the invention may express HLA-DR. Suitably, approximately 20 to 50%, approximately 20 to 45%, approximately 20 to 40%, approximately 20 to 35%, approximately 20 to 30%, approximately 20 to 25% of the cells of a population of cells of the invention may express HLA-DR. Suitably, approximately 25 to 50%, approximately 25 to 45%, approximately 25 to 40%, approximately 25 to 35%, approximately 25 to 30% of the cells of a population of cells of the invention may express HLA-DR. In a suitable embodiment, 20 to 40% of the cells of a population of cells of the invention may express HLA-DR. In one aspect, the present invention relates to a granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell may comprise: increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one aspect, the present invention relates to a granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell may comprise: decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one aspect, the present invention relates to a granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell may comprise: a. increased expression of one or more of: SRGN, MPO, HLA-DRA, CD74, and ELANE when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or b. decreased expression of one or more of: DEFA1, DEFA3, CAMP, BPI, and AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. In one (preferred) aspect, the present invention relates to a granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell comprises: a. increased expression of one or more of: SRGN, MPO, HLA-DRA, CD74, and ELANE when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and b. decreased expression of one or more of: DEFA1, DEFA3, CAMP, BPI, and AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. The term “increased expression” or “decreased expression” may mean increased and / or decreased expression of least 1 gene such as 1, 2, 3, 4, or 5, preferably at least 2 genes, preferably at least 3 genes, more preferably at least 4 genes, yet more preferably at least 5 genes. Most preferably, a granulocyte precursor cell may comprise increased expression of all of the listed genes and / or (preferably and) decreased expression of all the listed genes when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. The skilled person knows how to measure a gene expression level and determine if the expression level of one of more of the genes of the invention is increased or decreased in a cell of the invention (e.g. an in vitro differentiated granulocyte precursor cell) compared to an equivalent cell (e.g. a granulocyte precursor cell that has been differentiated in vivo.) using any known techniques in the art. Preferably, bulk RNA sequencing, e.g. as described herein. The granulocyte precursor cell that has been differentiated in vitro from a stem cell may be a granulocyte precursor cell that has been differentiated in vitro from any suitable stem cell. Preferably, the granulocyte precursor cell has been differentiated in vitro from a stem cell that has been derived or has been obtained from a (human) donor having granulocytes (neutrophils) with high cancer killing activity (CKA). The stem cell may be any suitable stem cells from the donor, such as HSCs and iPSC. Preferably the stem cells is an HSC. Preferably, the granulocyte precursor cell has been differentiated in vitro from an HSC that has been derived or has been obtained from a (human) donor having granulocytes (neutrophils) with high cancer killing activity (CKA). The CKA of a (preferably human) granulocytes (preferably neutrophils) obtained from a donor may be determined or measured by any suitable method (in vitro). Preferably, the CKA of the (preferably human) granulocytes (preferably neutrophils) is assessed by a method comprising: a. admixing granulocytes (preferably neutrophils) from a donor with cancer cells; b. incubating said admixture; and c. measuring the % of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (neutrophils). Measuring the % of cancer cells killed in step (c) may be performed as taught herein. A granulocyte (preferably a neutrophil) with high CKA may be a granulocyte (preferably a neutrophil) having a CKA of at least 30%, for instance at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95% or more. Preferably, a granulocyte (preferably a neutrophil) with high CKA is a granulocyte (preferably a neutrophil) having a CKA of at least 30%, preferably at least 50%, more preferably at least 70%. The equivalent granulocyte precursor cell that has been differentiated in vivo may be obtained from peripheral blood or from a cell bank. Preferably, the equivalent granulocyte precursor cell that has been differentiated in vivo is a peripheral blood derived granulocyte precursor cell. Preferably, the increased expression and / or decreased expression in one or more of the genes of the invention is not the result of a genetic modification of the granulocyte precursor cells (preferably promyelocytes, myelocytes and / or intermediate cells thereof). The term “serglycin (SRGN)” as used herein refers to a protein encoded by the SRGN gene in humans, known as a hematopoietic proteoglycan core protein or secretory granule proteoglycan core protein. SRGN typically functions as a scaffold protein in secretory granules of various immune cells, where it often helps in storing, secreting, and protecting proteases, chemokines, and other molecules. SRGN may be associated with the macromolecular complex of granzymes and perforin, which may serve as a mediator of granule-mediated apoptosis. The present inventors surprisingly found that SRGN was highly expressed in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because SRGN expression level was much higher than what is typically observed in natural (wild-type) cells (e.g. from human blood) of an equivalent developmental stage that have been differentiated in vivo or a cell of an equivalent developmental stage differentiated in vitro and obtained from a different method as evidenced for instance in: Korpetinou et al (2014) Frontiers in Oncology: Vol 3, Article 327, pages 1-12, available at: https: / / www.frontiersin.org / journals / oncology / articles / 10.3389 / fonc.2013.00327 / full). Without wishing to be bound by any theories, it is believed that such (relatively) high level of SRGN expression is indicative of cells (preferably granulocyte precursor cells) that are functionally primed as effector cells (e.g. activated cells capable of carrying out a specific response to eliminate threats like infections or abnormal cells such as cancer cells) enabling them to initiate cytotoxic or immunomodulatory responses at an earlier stage of maturation than typically observed. The term “myeloperoxidase (MPO)” as used herein refers to a heme-containing enzyme located in the azurophilic (primary) granules of neutrophils, where it typically contributes to antimicrobial defence by catalysing the production of reactive substances such as hypochlorous acid from hydrogen peroxide and chloride ions. Additionally, MPO typically plays a role in mediating cytotoxic activity, including the killing of abnormal cells like cancer cells, through the generation of potent reactive oxygen species (ROS). The present inventors surprisingly found that MPO was highly expressed in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because MOP expression level was much higher than what is typically observed in natural (wild-type cells, e.g. from human blood) of an equivalent developmental stage that have been differentiated in vivo or a cell of an equivalent developmental stage that have been differentiated in vitro and obtained from a different method as evidenced in e.g. Rizo-Téllez et al (2022) Vol 1(11), 2302, available at: https: / / www.mdpi.com / 2076- Without wishing to be bound by any theories, it is believed that the relatively high expression level of MPO is indicative of cells (preferably granulocyte precursor cells) equipped with antimicrobial and cytotoxic functions, thereby possessing an elevated cytocidal potential at an earlier stage of maturation than is typically observed. The term “major histocompatibility complex, class II, DR alpha (HLA-DRA)” as used herein refers to a major histocompatibility complex class II molecule. HLA-DRA is typically expressed on the surface of antigen-presenting cells, such as B lymphocytes, dendritic cells, and macrophages, and plays a critical role in immune function by presenting extracellularly derived peptide antigens to CD4+ T lymphocytes. The present inventors surprisingly found that HLA-DRA was highly expressed in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because HLA-DRA is not typically expressed in natural (wild type) granulocytes that have been differentiated in vivo, particularly it is not typically expressed in in vivo differentiated granulocyte precursors. Therefore, said high level of expression of HLA-DRA are unexpected, as evidenced in e.g. McKenna et al in: Frontiers in immunology (2021), Vol 12, Article 602963, available at: Without wishing to be bound by any theories, it is believed that such (relatively) high level of HLA-DRA expression is indicative of cells (preferably granulocyte precursor cells) that have acquired antigen-presenting cell–like properties, which is not a naturally-occurring phenomenon but rather is a property that is (likely) imparted to the cells of the invention by the methods and culture medium of the invention. The term “CD74” as used herein refers to a type II transmembrane glycoprotein commonly known as the invariant chain, which typically plays a critical role in the regulation of major histocompatibility complex class II (MHC II) molecule processing and trafficking within antigen-presenting cells. CD74 is typically expressed in antigen-presenting cells such as B cells, monocytes, macrophages, and dendritic cells. The present inventors surprisingly found that CD74 was highly expressed in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because CD74 is not typically expressed in in vivo differentiated granulocytes (typically not in in vitro differentiated granulocyte precursors), and when present on granulocytes (e.g. granulocyte precursor cells), its expression is generally very low or negligible, as evidenced for instance in the “Human Atlas” available at: Without any of CD74 expression is indicative of cells (preferably granulocyte precursor cells) that have acquired antigen-presenting cell–like properties, which is not a naturally-occurring phenomenon but rather is a property that is (likely) imparted to the cells of the invention by the methods and culture medium of the invention. The term “elastase (ELANE)” as used herein refers to a serine protease enzyme typically expressed in neutrophils, where it is stored in azurophil granules. ELANE typically plays a key role in innate immunity by degrading extracellular matrix proteins and microbial components, aiding in pathogen destruction. Additionally, ELANE exhibits selective cytotoxic activity against abnormal cells, including cancer cells, by inducing apoptosis. The present inventors surprisingly found that ELANE was highly expressed in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because ELANE expression level was much higher than what is typically observed in natural (wild-type cells, e.g. from human blood) of an equivalent developmental stage that have been differentiated in vivo or a cell of an equivalent developmental stage that have been differentiated in vitro and obtained from a different method. Without wishing to be bound by any theories, it is believed that the relatively high expression level of ELANE is indicative of cells (preferably granulocyte precursor cells) equipped with antimicrobial and cytotoxic functions, thereby possessing an elevated cytocidal potential at an earlier stage of maturation than is typically observed. The term “defensin alpha 1 (DEFA1)” as used herein refers to a small cationic antimicrobial peptide encoded by the DEFA1 gene and typically stored in the azurophil granules of neutrophils. DEFA1 belongs to the alpha-defensin family and exhibits broad-spectrum antimicrobial activities against bacteria, fungi, and viruses by disrupting pathogen membranes. In addition to its antimicrobial function, DEFA1 typically plays a role in cancer killing by selectively targeting and inducing apoptosis in tumour cells, thereby contributing to innate immune defence and tumour suppression. The present inventors found that DEFA1 was expressed at a (very) low level (or undetectable level) in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because DEFA1 expression level was much lower (was undetectable) than what is typically observed in (natural) wild-type cells (e.g. from human blood) of a comparable developmental stage differentiated in vivo or a cell of an equivalent developmental stage differentiated in vitro, obtained from a different method, as evidenced for instance in: Grassi et al in: Cell Reports (2018) Vol 24, pages 2784–2794, available at: https: / / www.cell.com / action / showPdf?pii=S2211-1247%2818%2931272-5). Without wishing to be bound by any theories, although the significance of low expression levels of DEFA1 is unknown, it is believed that such (relatively) low level of DEFA1 expression is indicative of cells that have acquired a distinct phenotype and / or gene marker profile that is not naturally occurring in cells of an equivalent developmental stage. The term “defensin alpha 3 (DEFA3)” as used herein refers to a small cationic antimicrobial peptide encoded by the DEFA3 gene and typically stored in the azurophil granules of neutrophils. DEFA3, also known as human neutrophil peptide 3 (HNP-3), is a member of the alpha-defensin family, differing from DEFA1 by a single amino acid. DEFA3 typically exhibits antimicrobial activity against bacteria, fungi, and viruses by disrupting microbial membranes, thus often playing a role in innate host defence. Similar to other alpha-defensins, DEFA3 may also contribute to immune modulation and cytotoxicity, supporting the elimination of pathogens and abnormal cells, such as cancer cells. The present inventors found that DEFA3 was expressed at a (very) low level (or undetectable level) in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because DEFA3 expression level was much lower (was undetectable) than what is typically observed in a natural cell (a wild-type cell, e.g. from human blood) a cell (preferably a granulocyte precursor cell) of an equivalent developmental stage that has been differentiated in vivo or a cell an equivalent developmental stage that has been differentiated in vitro and obtained from a different method, as evidenced for instance in: Grassi et al in: Cell Reports (2018) Vol 24, pages 2784–2794, available at: https: / / www.cell.com / action / showPdf?pii=S2211- 1247%2818%2931272-5). Without wishing to be bound by any theories, although the significance of low expression levels of DEFA3 is unknown, it is believed that such (relatively) low level of DEFA3 expression is indicative of cells that have acquired a distinct phenotype and / or gene marker profile that is not naturally occurring in cells of an equivalent developmental stage. The term “cathelicidin antimicrobial peptide (CAMP)” as used herein refers to a family of cationic antimicrobial peptides, including the human peptide LL-37, characterised by a conserved cathelin pro-domain and a diverse antimicrobial domain. Specifically, the CAMP gene encodes a precursor protein (hCAP18) that is processed to the active peptide LL-37. CAMP peptides are typically stored in granules of neutrophils and other immune cells and typically display broad-spectrum antimicrobial activity through membrane disruption and intracellular targeting of bacteria, fungi, and viruses. Beyond antimicrobial defence, CAMP peptides, such as LL-37, may also exhibit selective anticancer activity by inducing tumour cell death via membrane permeabilisation and modulation of immune responses. These peptides may also promote wound healing and inflammation regulation, making them multifunctional effectors of innate immunity with therapeutic potential in infectious diseases and cancer. The present inventors found that CAMP was expressed at a (very) low level (or undetectable level) in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because CAMP expression level was much lower (was undetectable) than what is typically observed in a natural cell (a wild-type cell e.g. from human blood) of an equivalent developmental stage that has been differentiated in vivo or a cell of an equivalent developmental stage differentiated in vitro and obtained from a different method, as evidenced for instance in: Nagaoka et al in: Journal of Leukocyte Biology (1998), Vol 64, Issue 6, pages 845–852, available at: abstract / 64 / 6 / 845 / 6977091?redirectedFrom=fulltext). Without wishing to be bound by any theories, although the significance of low expression levels of CAMP is unknown, it is believed that such (relatively) low level of CAMP expression is indicative of cells that have acquired a distinct phenotype and / or gene marker profile that is not naturally occurring in cells of an equivalent developmental stage. The term “bactericidal permeability increasing protein (BPI)” as sued herein refers to a neutrophil-derived, cationic protein encoded by the BPI gene, which typically plays a role in innate immunity by exhibiting potent antimicrobial activity against gram-negative bacteria. BPI typically binds to lipopolysaccharides in bacterial outer membranes, disrupting membrane integrity and causing bacterial death, while also acting as an opsonin to enhance phagocytosis and antigen presentation. In addition to its antimicrobial functions, BPI often contributes to anticancer activity by modulating immune responses and promoting tumour cell clearance. Thus, BPI is a multifunctional effector that may be involved in direct bacterial killing and immune system-mediated tumour suppression. The present inventors found that BPI was expressed at a (very) low level (or undetectable level) in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because BPI expression level was much lower (was undetectable) than what is typically observed in wild-type cells (e.g. from human blood) of a comparable developmental stage or a cell of a comparable developmental stage obtained from a different method, as evidenced for instance in: Lennartsson et al in: Journal of Leukocyte Biology (2006), Vol 80, Issue 1, pages 196–203, available at: Without wishing to be bound by any levels of BPI is unknown, it is believed that such (relatively) low level of BPI expression is indicative of cells that have acquired a distinct phenotype and / or gene marker profile that is not naturally occurring in cells of an equivalent developmental stage. The term “azurocidin 1 (AZU1)” as sued herein refers to a neutrophil-derived cationic glycoprotein encoded by the AZU1 gene that is typically stored in azurophil granules and secretory vesicles. AZU1 typically exhibits potent antimicrobial activity, particularly against gram-negative bacteria, through binding to lipopolysaccharides and disrupting bacterial membranes. Additionally, AZU1 may function as a multifunctional inflammatory mediator and chemotactic factor for monocytes and fibroblasts, promoting immune cell recruitment and vascular permeability. AZU1 may also exhibit anticancer activity. The present inventors found that AZU1 was expressed at a (very) low level (or undetectable level) in the cells of the invention, particularly in granulocyte precursors including promyelocytes, myelocytes or intermediate cells thereof. This is surprising because AZU1 expression level was much lower (was undetectable) than what is typically observed in a natural cell (e.g. a wild-type cell, e.g. from human blood) of an equivalent developmental stage that has been differentiated in vivo or a cell of an equivalent developmental stage that has been differentiated in vitro and obtained from a different method. Without wishing to be bound by any theories, although the significance of low expression levels of AZU1 is unknown, it is believed that such (relatively) low level of AZU1 expression is indicative of cells that have acquired a distinct phenotype and / or gene marker profile that is not naturally occurring in cells of an equivalent developmental stage. The genes of the invention (e.g. SRGN, MPO, HLA-DRA, CD74, ELANE, DEFA1, DEFA3, CAMP, BPI, and AZU1) have the following National Center for Biotechnology Information (NCBI) identification (ID) numbers as well as Ensembl_Gene_ID numbers. The skilled person knows how to determine a NCBI ID number and an Ensembl_Gene_ID number for a given gene by, for instance, searching the NCBI gene database at: and Ensembl_Gene_ID database at: Table X: NCBI Gene ID Numbers Genes NCBI Gene ID Ensembl_Gene_ID Numbers Serglycin (SRGN) 5552 ENSG00000122862 Myeloperoxidase (MPO) 4353 ENSG00000005381 MHC class II, DR alpha 3122 ENSG00000204287 (HLA-DRA) CD74 (CD74) 972 ENSG00000019582 Neutrophil Elastase 1991 ENSG00000197561 (ELANE) Defensin alpha 1 1667 ENSG00000206047 (DEFA1) Defensin alpha 3 1668 ENSG00000239839 (DEFA3) Cathelicidin antimicrobial 820 ENSG00000164047 peptide (CAMP) Bactericidal / Permeability- 671 ENSG00000101425 Increasing Protein (BPI) Azurocidin 1 (AZU1) 566 ENSG00000172232 The gene version relating to the NCBI Gene ID Numbers and Ensembl_Gene_ID listed in the Table represents the latest available as of 19 September 2025 for both. The granulocyte precursor cell may be one of: a common myeloid progenitor cell, a myeloblast, a neutrophil promyelocyte, a neutrophil myelocyte, a neutrophil metamyelocyte, a neutrophil band, an intermediate cell thereof or any combinations thereof. The granulocyte precursor cell may be a promyelocyte, a myelocyte, or an intermediate thereof. Preferably, the granulocyte precursor cell of the invention (differentiated in vitro) is a promyelocyte, a myelocyte, or an intermediate thereof. Preferably, the granulocyte precursor cell of the invention (differentiated in vitro) is a promyelocyte, a myelocyte, or an intermediate thereof or any combinations thereof. Properties of granulocytes, or precursors thereof, within the cell populations of the invention Cells of the invention exert cytocidal activity. They are able to exert this cytocidal activity in respect of pathological cells (such as cancer cells or infected cells) and thereby provide treatment of diseases caused by such pathological cells. Cells of the invention exhibit immunomodulatory activity. This immunomodulatory activity may therapeutically modulate an immune response (for example amplifying or dampening an immune response) to improve its therapeutic efficacy. Medical uses and methods of treatment utilising the cells of the invention are considered in more detail elsewhere in the specification. The benefits provided by the methods of the invention, and by the cells of the invention produced by such methods, are described further elsewhere in this specification (for example in the detailed description of the invention, and in the Examples). These benefits give rise to many advantageous uses of the cells of the invention. Cryopreservation concentrations suitable for use in the methods of the invention Suitably, the cryopreservation concentration is approximately 5E6 – 50E6 cells / ml. In a suitable embodiment, the cryopreservation concentration is approximately 10E6 cells / ml. In a suitable embodiment, the cryopreservation concentration is approximately 40E6 cells / ml. Optional processing of cells of the invention The populations of granulocytes, or precursors thereof (e.g. granulocyte precursor), produced by the methods of the invention may optionally be harvested once produced. For the purposes of the present disclosure, “harvesting” of cells may be taken to encompass suspension of the cells, isolation of the cells, or separation of the cells. The populations of granulocytes, or precursors thereof (e.g. granulocyte precursor), produced by the methods of the invention may optionally be cryopreserved once produced. It is known that granulocytes, such as neutrophils, do not respond well to cryopreservation, with low levels of viable cells remaining after a frozen population of cells has been thawed. In contrast, the granulocytes, or precursors thereof (e.g. granulocyte precursor), of the present invention are well adapted to cryopreservation, with high levels of viable cells being obtained after the freezing and thawing process. Accordingly, the granulocytes, or precursors thereof (e.g. granulocyte precursor), of the invention offer significant advantages, as compared to mature granulocytic cells (e.g. neutrophils), in applications in which it is desired to cryopreserve cells before their use for therapy. The populations of granulocytes, or precursors thereof (e.g. granulocyte precursors), produced by the methods of the invention may optionally be formulated for medical use once produced. Methods suitable for formulation of cell populations that are to be used therapeutically will be well known to those skilled in the art, and may be used in the formulation of the granulocyte, or precursors thereof (e.g. granulocyte precursors), populations of the invention, optionally to give rise to pharmaceutical compositions of the invention. Pharmaceutical compositions of the invention The eighth aspect of the invention provides a pharmaceutical composition comprising a population of cells of the invention. Suitably, the population of cells may be in accordance with any of the fourth to seventh aspects of the invention. A pharmaceutical composition of the invention may comprise a pharmaceutically acceptable carrier, excipient, or diluent, in addition to the population of cells of the invention. A pharmaceutical composition of the invention may, for example, be formulated for administration to a subject by injection or infusion. A pharmaceutically acceptable carrier may be an injectable carrier, such as a sterile physiological saline solution. In one aspect, the invention provides a pharmaceutical composition comprising the (in vitro differentiated ) granulocyte precursor cells of the invention as taught herein. The pharmaceutical composition may further comprise G-CSF. Preferably, the pharmaceutical composition comprises G-CSF. The pharmaceutical composition may comprise further suitable excipients. The pharmaceutical may be cryoprotected. Dosage and administration An appropriate dosage range of a population of cells of the invention, or of a pharmaceutical composition of the invention, is one that produces the desired therapeutic effect when provided to a recipient. An appropriate dosage range may be achieved by a single incidence of administration, or by multiple incidences of administration. Administration may be by any suitable technique or route, including but not limited to intravenous injection, intra-arterial injection, intraperitoneal injection, injection into a tumour resection cavity, intrathecal injection, or combinations thereof. Suitably the medicament may be administered intravenously. A typical treatment regimen may include administering from 106, 107, 108or 109cells (e.g. cells of a population of granulopoietic cells (preferably a population of granulocyte precursor cells as taught herein) to a subject, or up to 1012, 1013or 1014cells to a subject. In a suitable embodiment a treatment regimen includes administering a dose of at least 1 x 109cells to a subject. Suitably, a treatment regimen may include administering a dose of at least 2 x 109cells or at least 5 x 109cells to a subject. In a suitable embodiment a treatment regimen may include administering a dose of at least 1 x 1010cells or at least 5 x 1010cells to a subject. At least 1 x 1011or at least 2 x 1011cells may be administered to a subject. In some embodiments between 1 x 109to 3 x 1011or 1 x 1010to 3 x 1011cells are administered to a subject. Suitably, between 5 x 1010to 2.5 x 1011cells are administered to a subject. A subject for treatment may be dosed once, twice, three times, four times, five times, or six times per week. Alternatively, a subject may be dosed daily (e.g. once or twice daily). In other embodiments a subject may be dosed once weekly or bi-weekly. Preferably the dose is weekly. The skilled person will appreciate that the dose can be tailored based on the needs of the subject, and efficacy of the medicament. For example, where the medicament is highly efficacious, the dose may be lowered. In a suitable embodiment a subject for treatment is dosed weekly (e.g. once weekly) with at least 2 x 109cells or at least 2 x 1010cells. Suitably, a subject for treatment may be dosed weekly with at least 1 x 1011or at least 2 x 1011cells. The treatment term can be varied based on the response of the subject to the treatment, and / or the type and / or severity of the disorder (e.g. cancer or infection). For example, the subject for treatment may be dosed for at least 1 or 2 weeks. Suitably the subject for treatment may be dosed for at least 3 or 4 weeks. In a suitable embodiment the subject for treatment is dosed for at least 5 or 6 weeks, suitably at least 7 or 8 weeks. In a suitable embodiment a subject for treatment is dosed for 4-8 weeks with at least 2 x 109cells, wherein said cells are administered once weekly. Suitably a subject for treatment is dosed for 8 weeks with at least 2 x 109cells (preferably at least 2 x 1010or 2 x 1011cells), wherein said cells are administered once weekly. The term a “subject” as used herein refers to a mammal. A subject may be a non-murine mammal. A subject may be a livestock mammal, a domesticated mammal, such as a pet, or a wildlife species. A subject may be a human, a horse, a monkey, a cow (including a bull), a pig, a dog, a cat, a sheep, a goat, an elephant, a panda, a mouse, a rabbit, a rat, or other mammal. Preferably “subject” means a human subject (also referred to as a patient), a horse, or a cow. Most preferably a subject is a human subject. A “subject” may be an adult or a child (younger than 18 years of age). Preferably, the subject is an adult subject, e.g. a human subject of at least 18 years old. The terms “subject” and “patient” may be used synonymously herein. A subject may be a subject having a disorder as defined herein, e.g. a cancer or an infection or an autoimmune disease. The term “treat” or “treating” as used herein may encompass prophylactic treatment (e.g. to prevent onset of a disorder or a symptom thereof) as well as corrective treatment (e.g. treatment of a subject already suffering from a disorder or a symptom thereof). Prophylactic treatment may also be referred to as preventive treatment. The term “disorder” as used herein may also encompass a “disease”. For example, the disorder may be a disease. A granulocyte and / or precursor, population of cells, or (pharmaceutical) composition of the invention may be administered to a subject in a therapeutically effective amount or a prophylactically effective amount. A “therapeutically effective amount” may be any amount of granulocyte and / or precursor, population of cells, or (pharmaceutical) composition of the invention, which when administered alone or in combination with another agent (preferably alone) to a subject for treating a disorder (or a symptom thereof) is sufficient to effect such treatment of the disorder, or symptom thereof. A “prophylactically effective amount” is any amount of the granulocyte and / or precursor, population of cells, or (pharmaceutical) composition that, when administered alone or in combination with another agent (preferably alone) to a subject inhibits or delays the onset or reoccurrence of a disorder (or a symptom thereof). In some embodiments, the prophylactically effective amount prevents the onset or reoccurrence of a disorder or symptom thereof entirely. “Inhibiting” the onset means either lessening the likelihood of a disorder’s onset (or symptom thereof), or preventing the onset entirely. Embodiments related to the various methods of the invention are intended to be applied equally to other methods, the granulocytes and / or precursors thereof, populations of cells, compositions, pharmaceutical compositions, kits, or uses, and vice versa. Medical uses and methods of treatment of the invention As set out above, populations of cells of the invention (preferably the granulocyte precursor cells of the invention), or pharmaceutical compositions of the invention, are suitable for use as medicaments, or in methods of treatment. The following provides examples of some of the medical uses (or methods of treatment) in which the populations of cells of the invention, or pharmaceutical compositions of the invention, may be employed. Cells of the invention may exert cytocidal activity (e.g. in vitro and / or in vivo) that can be used therapeutically. Cells of the invention may exert immunomodulatory activity (e.g. in vitro and / or in vivo) that can be used therapeutically. The cells and pharmaceutical compositions of the invention may be used in the treatment of a wide range of disorders. Suitably the cells (preferably the granulocyte precursor cells of the invention) and pharmaceutical compositions of the invention may be used in the treatment of cancer, infections, or autoimmune diseases. Cytocidal activity in medical uses As described elsewhere in the specification, the cells of the invention are able to exert cytocidal activity in respect of target cells. This cytocidal activity can kill pathological cells, such as cancer cells or infected cells, to provide a therapeutic effect. The methods of the invention beneficially give rise to populations of cells of the invention that have elevated cytocidal activity as compared to in vitro differentiated granulocytes or precursors thereof (e.g. granulocyte precursors) of an equivalent developmental stage produced by alternative means or compared to natural (wild type) in vivo differentiated granulocytes or precursors thereof (e.g. granulocyte precursors) of an equivalent developmental stage isolated from blood (e.g. human blood). The term “cytocidal activity” as use herein in the context of the cells of the invention (granulocyte precursors cells) refers to the ability of these cells to actively kill target cells by inducing damage leading to cell death, thereby eliminating undesired or harmful cells (e.g. cancer cells or pathogens like viruses, bacteria, etc) typically through biological actions characteristic of granulocyte lineage cells, such as phagocytosis, degranulation, and production of cytotoxic mediators. Suitably, a cell of the invention, or population of cells of the invention (preferably, the granulocyte precursor cells of the invention), may be able to kill at least 5% of a population of target cells (such as cancer cells or infected cells). Suitably, a cell of the invention, or population of cells of the invention, may be able to kill at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, or even 100% of a population of target cells (such as cancer cells or infected cells). Such cytocidal activity referred to in the preceding paragraph may be the activity of cells of the invention alone, or of cells of the invention in combination with other cells of the immune system that respond to signals from the cells of the invention. Immunomodulatory medical uses In one aspect, the invention provides a method of treatment comprising amplifying a non- granulocytic therapeutic immune response, the method comprising providing a population of cells of the invention (preferably the granulocyte precursors of the invention), or pharmaceutical composition of the invention, to a subject in need of such treatment. In the Examples, the inventors have demonstrated that cells of the invention are able to amplify immune responses through a number of different mechanisms. In particular, the cells of the invention may increase activation of immune cells, and increase activities (such as cell trafficking and cytocidal activity) required to achieve a successful therapeutic immune response. A therapeutic immune response may involve the action of any cells of the immune system. A “non-granulocytic immune response” may involve the action of any cells of the immune system, other than granulocytes. Merely by way of example, a therapeutic immune response that may be amplified by the medical uses, methods of treatment, or pharmaceutical compositions of the invention may involve the action of one or more cell types selected from the group consisting of: T cells (including, but not limited to CD8+T cells; CD4+T cells; NK T cells; αβ T cells; γδ T cells; peripheral blood T cells; and tumour infiltrated T cells); NK cells; monocytes; macrophages; dendritic cells (DCs); and B cells. It will be appreciated that it is activated immune cells that are primarily responsible for providing the desired activity in a therapeutic immune response. Accordingly, the ability of the medical uses and methods of treatment to increase activation of immune cells will be of benefit in almost all circumstances in which a therapeutically effective immune response is required. In particular, the amplification of a therapeutic immune response by increasing activation of immune cells may, without limitation, be advantageous in the treatment of cancer or the treatment of infections. Without wishing to be bound by any hypothesis, the increase in abundance of immune cells observed on exposure of such cells to cells of the invention may arise as a result of a combination of the increased proliferation and increase survival of the immune cells discussed in more detail above. However it arises, it offers real benefits in terms of the medical uses and methods of the invention. By increasing the abundance of immune cells able to take part in a therapeutic immune response, the medical uses and methods of treatment of the invention have the capacity to amplify such a therapeutic immune response both in terms of its extent and its duration. This will clearly provide benefits in many therapeutic contexts. Many of the properties of the cells suitable for use in the medical uses and methods of the invention indicate that these cells are also well suited to use in combination with other cell therapies, and in particular for use with further cell immunotherapies. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention for use as a medicament. In one aspect, the invention provides for the use a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in the manufacture of a medicament. In one aspect, the invention provides for a method for treating a disorder comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention for use in treating cancer. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in the manufacture of a medicament for treating cancer. In one aspect, the invention provides for a method for treating cancer comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention. The cancer may be one or more of: head and neck cancer, cervical cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach cancer, cervical cancer, ovarian cancer, lung cancer, bladder cancer, kidney cancer, brain cancer, prostate cancer, myeloma cancer, non-Hodgkin’s lymphoma (NHL), larynx cancer, uterine cancer, or breast cancer. Preferably the cancer is head and neck cancer and / or cervical cancer. Combination therapies In some embodiments a population of cells of the invention or pharmaceutical composition of the invention may be used in combination with another therapeutic, e.g. in combination with an existing cancer or infection therapy, such as radiotherapy, chemotherapy, and / or immunotherapy. By way of example, a population of cells of the invention, or pharmaceutical composition of the invention, may be used in combination with a cell engaging therapy, such as a T cell engaging therapy. Examples of such therapies that may be used in combination with a population of cells of the invention, or pharmaceutical composition of the invention,include those selected from the group comprising (or consisting) of: bispecific T cell engagers (BiTEs); checkpoint-inhibitory T cell engagers (CiTEs); simultaneous multiple interaction T cell engagers (SMiTEs); trispecific killer engagers (TriKEs); and BiTE-expressing CAR-T cells (CART.BiTE cells). In particular, the finding that populations of cells of the invention, or pharmaceutical compositions of the invention, are able to increase expression by immune cells of costimulatory molecules such as 4-1BB and OX40, suggests that they may advantageously be used in combination with T cell engaging therapies such as mono / bispecific 4-1BB agonists, or TAA / 4-1BB bispecific T cell engagers, or mono / bispecific OX40 agonists. The cells of the invention express markers indicating their capacity for activation, and also their capacity to activate other cells of the immune system. The marker profile expressed by the cells of the invention suggest that it may be possible to beneficially combine the cells of the invention, with mono / bispecific antibodies that activate innate immune cells. For example, cells of the invention may suitably be used in combination with anti-CD40 antibodies or anti-CD40 / TAA bispecific antibodies for combined granulopoietic cell activation and tumour targeting. A population of cells of the invention, or a pharmaceutical composition of the invention, may be used in combination with an immune cell engager. Merely by way of example, a suitable immune cell engager may be a bispecific T cell engager, or a combination molecule providing a checkpoint inhibitor in combination with a T cell engager. Examples of such molecules include OX40x4-1BB (produced by F-star, and designated FS120) or PD-L1x4-1BB (also produced by F-star, and designated FS222). Populations of cells of the invention, or pharmaceutical compositions of the invention, may be used in combination with one or more checkpoint inhibitors. By way of example, a suitable checkpoint inhibitor may be an inhibitor of PD-L1, such as Atezolizumab, Avelumab, Cemiplimab, or Durvalumab. Alternatively, or additionally, a suitable checkpoint inhibitor may be an inhibitor of CTLA-4, such as Ipilimumab. A suitable checkpoint inhibitor may be an inhibitor of PD-1, such as Nivolumab or Pembrolizumab. In another embodiment a suitable checkpoint inhibitor may be an inhibitor of LAG-3, such as Relatlimab. In a suitable embodiment, a population of cells of the invention, or a pharmaceutical composition of the invention, may be used in combination with one or more antibodies to a TAA. Preferably, the antibodies may be able to bring about cell death via antibody- dependent cellular cytoxicity (ADCC). Suitable examples of such antibodies include those selected from the group consisting of: Alemtuzumab (an anti-CD52 antibody); Avelumab (an anti-PD-L1 antibody); Cetuximab (an anti-EGFR antibody); Daratumumab (an anti-CD38 antibody); Dinutuximab (an anti-GD2 antibody); Elotuzumab (an anti-SLAMF7 antibody); Isatuximab (an anti-CD38 antibody); Margetuximab (an anti-HER2 antibody); Mogamulizumab (an anti-CCR4 antibody); Naxatamab (an anti-GD2 antibody); Necitumumab (an anti-EGFR antibody); Ofatumumab (an anti-CD20 antibody); Pertuzumab (an anti-HER2 antibody); Rituximab (an anti-CD20 antibody); Tafasitamab (an anti-CD19 antibody); and Trastuzumab (an anti-HER2 antibody). A population of cells of the invention, or a pharmaceutical composition of the invention, may be used in combination with a bispecific engager with Fc-mediated function, such as Amivantamab (EGFR x Met). Combination therapies with adoptive immunotherapies The inventors have identified that the pharmaceutical compositions or population of cells of the invention, are well suited for use in combination with an adoptive immunotherapy cell. Suitably, the adoptive immunotherapy cell expresses a chimeric antigen receptor (CAR). Such an adoptive immunotherapy cell may be a CAR-T cell. These combined uses with adoptive immunotherapy cells may be of benefit in the treatment of cancer. The cancer may comprise a solid tumour. Details of cancers that may be treated using the cells or pharmaceutical compositions of the invention are described elsewhere in the specification. Unless context requires otherwise, such cancers may be treated by means of combination therapy with an adoptive immunotherapy cell. A pharmaceutical composition, or population of cells, of the invention may be used in combination therapy with an adoptive immunotherapy cell expressing a CAR specific for a TAA as described above. Alternatively, or additionally, a pharmaceutical composition, or population of cells, of the invention may be used in combination therapy with an adoptive immunotherapy cell expressing a CAR specific for a TAA selected from the group consisting of: prostate specific membrane antigen (PSMA), carcinoembryonic antigen (CEA), IL13Ralpha, HER-2, CD19, NY - ESO-1, HIV-1 Gag, Lewis Y, MART-1, gp100, tyrosinase, WT-I, hTERT, mesothelin, EGFR, EGFRvIII, phosphatidylinositol 3, EphA2, HER3, EpCAM, MUC1, MUC16, Folate receptor, CLDN6, CD30, CD138, ASGPR1, CDH16, GD2, 5T4, 8H9, avß6 integrin, B cell mature antigen (BCMA), B7 - H3, B7 - H6, CAIX, CA9, CD20, CD22, K Kappa light chain, CD33, CD38, CD44, CD44v6, CD44v7 / 8, CD70, CD123, CD171, CSPG4, EGP2, EGP40, ERBB3, ERBB4, ErbB3 / 4, FAP, FAR, FBP, embryonic AchR, GD2, GD3, HLA - AI MAGE A1, MAGE3, HLA - A2, IL11Ra, KDR, Lambda, MCSP, NCAM, NKG2D ligand, PRAME, PSCA, PSC1, ROR1, Sp17, SURVIVIN, TAG72, TEM1, TEM8, VEGRR2, HMW - MAA, VEGF receptor, and fibronectin, tenascin or carcinoembryonic variants of tumour necrotic regions. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing therapeutic activity of the adoptive immunotherapy cell. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing activation of the adoptive immunotherapy cell. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by reducing CAR-down regulation on target engagement by the adoptive immunotherapy cell. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing accumulation of adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing proliferation of the adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing persistence of the adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing survival of the adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing cytotoxic activity of the adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by decreasing T cell exhaustion of immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided in a smaller number than the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided in approximately the same number as the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided in a greater number than the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided prior to the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided after the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided at approximately the same time as the adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are formulated in combination with the adoptive immunotherapy cells. The populations of cells of the invention, or pharmaceutical compositions of the invention, may be in accordance with any of the embodiments described in this specification. Suitably a subject receiving treatment by means of a medical use or method of treatment of the invention may be a patient with cancer. A suitable patient may have any form of cancer, including those described further in this disclosure. For example, a patient may have pancreatic cancer. Suitably a subject receiving treatment by means of a medical use or method of treatment of the invention may be a patient with an infection. A suitable patient may have any form of infection, including those described further in the present disclosure. Merely by way of example, a patient may have a viral infection. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention, or a pharmaceutical composition of the invention, in combination with a CAR-T cell. Said combination therapy may be used for the treatment of any disorder. Preferably, the disorder is cancer. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in combination with an antibody. Said combination therapy may be used for the treatment of any disorder. Preferably, the disorder is cancer. The antibody may be selected from: Cetuximab, Rituximab, Daratumumab, Tafasitamab, Obinutuzumab, Ofatumumab, Alemtuzumab, Blinatumomab, Lynozyfic, Panitumumab, Bevacizumab, Ramucirumab, Denosumab, Dinutuximab, and Elotuzumab. Preferably, the antibody is Cetuximab. Said combination therapy may be used for the treatment of any disorder. Preferably, the disorder is cancer. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in combination with an immune check point inhibitor. Said combination therapy may be used for the treatment of any disorder. Preferably, the disorder is cancer. The check point inhibitor may be selected from: Nivolumab, Ipilimumab, Pembrolizumab, Cemiplimab, Durvalumab, Atezolizumab, Relatlimab, Dostarlimab, Avelumab, Tislelizumab, Toripalimab, Sugemalimab, Camrelizumab, and Tremelimumab. Preferably, the check point inhibitor is Nivolumab. The cancer may be selected from head and neck cancer, cervical cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach cancer, cervical cancer, ovarian cancer, lung cancer, bladder cancer, kidney cancer, brain cancer, prostate cancer, myeloma cancer, non- Hodgkin’s lymphoma (NHL), larynx cancer, uterine cancer, and breast cancer. Preferably, the cancer is head and neck cancer and / or cervical cancer. Treatment of cancer Suitably, the invention provides the use of a population of cells of the invention, or pharmaceutical composition of the invention, for treating cancer in a subject. Suitably, the invention provides use of a population of cells of the invention, or pharmaceutical composition of the invention, in the manufacture of a medicament for treating cancer in a subject. The medical uses, methods of treatment or compositions (e.g. pharmaceutical compositions) of the invention may all be employed in the treatment of cancer. Cancer may be treated by killing or otherwise therapeutically reducing the activity of cancer cells. This may occur as a result of the activity of the cells of a population of cells of the invention, or pharmaceutical composition of the invention, or the progeny of such cells. Alternatively, or additionally, this may occurs as a result of immunomodulation by a population of cells of the invention, or pharmaceutical composition of the invention, to provide a therapeutically effective immune response. In a suitable embodiment a cancer to be treated is a solid tumour cancer. The term “solid tumour cancer” refers to an abnormal, malignant mass of tissue that does not contain cysts or liquid inclusions. Examples of solid tumour cancers include carcinomas, sarcomas, and lymphomas. A solid tumour cancer may be a carcinoma. A carcinoma may be selected from one or more of an adenocarcinoma, a basal cell carcinoma, a squamous cell carcinoma, an adenosquamous carcinoma, a renal cell carcinoma, a ductal carcinoma in situ (DCIS), an invasive ductal carcinoma, an anaplastic carcinoma, a large cell carcinoma, a small cell carcinoma or combinations thereof. A carcinoma may also be selected from epithelial neoplasms, squamous cell neoplasms, squamous cell carcinoma, basal cell neoplasms, basal cell carcinoma, transitional cell carcinomas, adenocarcinomas (such as Adenocarcinoma not otherwise specified (NOS), linitis plastica, vipoma, cholangiocarcinoma, hepatocellular carcinoma NOS, adenoid cystic carcinoma, renal cell carcinoma, Grawitz tumour), adnexal and skin appendage neoplasms, mucoepidermoid neoplasms, cystic mucinous and serous neoplasms, ductal lobular and medullary neoplasms, acinar cell neoplasms, or complex epithelial neoplasms. Alternatively, a solid tumour cancer may be a sarcoma. A sarcoma may be selected from Askin's tumour, sarcoma botryoides, chondrosarcoma, Ewing's, malignant hemangioendothelioma, malignant schwannoma, osteosarcoma, or soft tissue sarcomas (including alveolar soft part sarcoma, angiosarcoma, cystosarcoma phyllodes, dermatofibrosarcoma protuberans (DFSP), desmoid tumour, desmoplastic small round cell tumour, epithelioid sarcoma, extraskeletal chondrosarcoma, extraskeletal osteosarcoma, fibrosarcoma, gastrointestinal stromal tumour (GIST), hemangiopericytoma, hemangiosarcoma, Kaposi's sarcoma, leiomyosarcoma, liposarcoma, lymphangiosarcoma, malignant fibrous histiocytoma, undifferentiated pleomorphic sarcoma, malignant peripheral nerve sheath tumour (MPNST), neurofibrosarcoma, rhabdomyosarcoma, and synovial sarcoma). Alternatively, a solid tumour may be a lymphoma, such as a B-cell lymphoma, a T-cell lymphoma, a NK-cell lymphoma, or a Hodgkin’s lymphoma. In a suitable embodiment, a medical use, method of treatment, or composition (e.g. pharmaceutical composition) of the invention is for use in treating one or more of: pancreatic cancer, liver cancer, oesophageal cancer, stomach cancer, cervical cancer, ovarian cancer, lung cancer, bladder cancer, kidney cancer, brain cancer, prostate cancer, myeloma cancer, non-Hodgkin’s lymphoma (NHL), larynx cancer, uterine cancer, or breast cancer. In the case that the medical use, method of treatment, or composition (e.g. pharmaceutical composition) of the invention is for use in treating pancreatic cancer, the pancreatic cancer may be a pancreatic solid tumour cancer, such as a pancreatic adenocarcinoma (e.g. a pancreatic ductal adenocarcinoma). Treatment of infections Suitably, the invention provides use of a population of cells of the invention, or pharmaceutical composition of the invention, as a medicament for treating an infection in a subject. Suitably, the invention provides use of a population of cells of the invention, or pharmaceutical composition of the invention, in the manufacture of a medicament for treating an infection in a subject. The medical uses, methods of treatment, or compositions (e.g. pharmaceutical compositions) of the invention may all be employed in the treatment of infections. Such infections may be treated by killing or otherwise therapeutically reducing the activity of infectious agents (such as cellular infectious agents), or by killing or otherwise therapeutically reducing the activity of cells infected by infectious agents. As used herein, a “cell infected by an infective agent” refers to a cell that is infected by an intracellular infective agent. Said intracellular infective agent may be a pathogen and the cell is therefore a “cell infected by a pathogen”. In a suitable embodiment a cell may be infected by an intracellular bacterium or a virus, preferably a virus. In a suitable embodiment an infection to be treated is caused by a Gram-negative bacterium or a Gram-positive bacterium. Preferably, an infective agent is a Gram-positive bacterium, such as a bacterium from the genus Staphylococcus. Suitably an infection to be treated is caused by a bacterium selected from one or more of Staphylococcus spp., multidrug resistant gram-negative bacteria (MRDGN bacteria), vancomycin-resistant Enterococcus (VRE), Mycobacterium spp., carbapenem-resistant Enterobacteriaceae (CRE) gut bacteria, Acinetobacter spp., Actinomyces spp., Propionibacterium spp., Anaplasma spp., Bacillus spp., Arcanobacterium spp., Bacteroides spp., Bartonella spp., Brucella spp., Yersinia spp., Burkholderia spp., Campylobacter spp., Streptococcus spp., Haemophilus spp., Clostridium spp., Corynebacterium spp., Echinococcus spp., Ehrlichia spp., Enterococcus spp., Rickettsia spp., Fusobacterium spp., Neisseria spp., Klebsiella spp., Helicobacter spp., Escherichia spp., Kingella spp., Legionella spp., Listeria spp., Borrelia spp., Mycoplasma spp., Chlamydia spp., Nocardia spp., Pasteurella spp., Bordetella spp., Prevotella spp., Chlamydophila spp., Coxiella spp., Salmonella spp., Group A Streptococcus spp., Shigella spp., Staphylococcus spp., Treponema spp., Vibrio spp., Francisella spp., Pseudomonas spp. and Ureaplasma spp. In a suitable embodiment the bacterium is selected from one or more of methicillin resistant Staphylococcus aureus (MRSA), multi-drug resistant Mycobacterium tuberculosis (MDR- TB), Pseudomonas aeruginosa, Pseudomonas oryzihabitans, Pseudomonas plecoglossicida, Acinetobacter baumannii, Actinomyces israelii, Actinomyces gerencseriae, Propionibacterium propionicus, Bacillus anthracis, Arcanobacterium haemolyticum, Bacillus cereus, Yersinia pestis, Mycobacterium ulcerans, Campylobacter jejuni, Bartonella bacilliformis, Bartonella henselae, Haemophilus ducreyi, Clostridium difficile, Corynebacterium diphtheria, Burkholderia mallei, Neisseria gonorrhoeae, Klebsiella granulomatis, Streptococcus pyogenes, Streptococcus agalactiae, Haemophilus influenzae, Helicobacter pylori, Escherichia coli (e.g. O157:H7, O111 and O104:H4), Kingella kingae, Legionella pneumophila, Listeria monocytogenes, Burkholderia pseudomallei, Neisseria meningitidis, Mycoplasma pneumoniae, Mycoplasma genitalium, Chlamydia trachomatis, Bordetella pertussis, Streptococcus pneumoniae, Chlamydophila psittaci, Coxiella burnetii, Treponema pallidum, Clostridium tetani, Chlamydophila pneumoniae, Vibrio cholera, Mycobacterium tuberculosis, Salmonella enterica subsp. enterica, serovartyphi, Ureaplasma urealyticum, and Francisella tularensis. Preferably Mycobacterium tuberculosis. Preferably, in a suitable embodiment the bacterium is selected from one or more of methicillin resistant Staphylococcus aureus (MRSA), multidrug resistant gram-negative bacteria (MRDGN bacteria), vancomycin-resistant Enterococcus (VRE), multi-drug resistant Mycobacterium tuberculosis (MDR-TB), and carbapenem-resistant Enterobacteriaceae (CRE) gut bacteria. Suitably an infection to be treated is caused by a virus selected from one or more family selected from Adenoviridae, Picornaviridae, Herpesviridae, Coronaviridae, Hepadnaviridae, Flaviviridae, Retroviridae, Orthomyxoviridae, Paramyxoviridae, Papovaviridae, Polyomavirus, Rhabdoviridae, Togaviridae and Bunyaviridae. In a suitable embodiment the virus may be selected from one or more of HIV-1 (Human immunodeficiency virus), HIV-2, Junin virus, BK virus, Machupo virus, Sabiá virus, Varicella zoster virus (VZV), Alphavirus, Colorado tick fever virus (CTFV), Rhinoviruses, Crimean- Congo hemorrhagic fever virus, Cytomegalovirus, Dengue virus, Ebolavirus (EBOV), Parvovirus B19, Human herpesvirus 6 (HHV-6), Human herpesvirus 7 (HHV-7), Enteroviruses (e.g. EV71), Coxsackie A virus, Sin Nombre virus, Heartland virus, Hanta virus, Hendra virus, Hepatitis A virus, Hepatitis B virus, Hepatitis C virus, Hepatitis D Virus, Hepatitis E virus, Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), Human bocavirus (HBoV), Human metapneumovirus (hMPV), Human papillomaviruses, Human parainfluenza viruses (HPIV), Epstein–Barr virus (EBV), Lassa virus, Lymphocytic choriomeningitis virus (LCMV), Marburg virus, Measles virus, Middle East respiratory syndrome coronavirus, Molluscum contagiosum virus (MCV), Monkeypox virus, Mumps virus, Nipah virus, Norovirus, Poliovirus, JC virus, Respiratory syncytial virus (RSV), Rhinovirus, Rift Valley fever virus, Rotavirus, Rubella virus, SARS coronavirus, SARS-CoV-2, Variola major, Variola minor, Venezuelan equine encephalitis virus, Guanarito virus, West Nile virus, Yellow fever virus, and Zika virus. Suitably an infection to be treated is caused by a fungus selected from one or more of Aspergillus spp., Piedraia spp., Blastomyces spp., Candida spp., Fonsecaea spp., Coccidioides spp., Cryptococcus spp., Cryptosporidium spp., Geotrichum spp., Histoplasma spp., Microsporidia phylum, Paracoccidioides spp., Pneumocystis spp., Sporothrix spp., Trichophyton spp., Epidermophyton spp., Hortaea spp., Malassezia spp., Trichosporon spp., and Mucorales order. In a suitable embodiment the pathogen is a fungus selected from one or more of Aspergillus fumigatus, Aspergillus flavus, Piedraia hortae, Blastomyces dermatitidis, Candida albicans, Fonsecaea pedrosoi, Coccidioides immitis, Coccidioides posadasii, Cryptococcus neoformans, Geotrichum candidum, Histoplasma capsulatum, Paracoccidioides brasiliensis, Pneumocystis jirovecii, Sporothrix schenckii, Trichophyton tonsurans, Epidermophyton floccosum, Hortaea werneckii, and Trichosporon beigelii. A macroparasite may be one or more selected from Angiostrongylus spp., Entamoeba Anisakis spp., Ascaris spp., Babesia spp., Balantidium spp., Baylisascaris spp., Blastocystis spp., Capillaria spp., Trypanosoma spp., Clonorchis spp., Ancylostoma spp., Cyclospora spp., Taenia spp., Desmodesmus spp., Dientamoeba spp., Dracunculus spp,. Enterobius spp., Fasciola spp., Filarioidea superfamily, Giardia spp., Gnathostoma spp., Necator spp., Hymenolepis spp., Isospora spp., Leptospira spp., Wuchereria spp., Rhinosporidium spp., Brugia spp., Plasmodium spp., Onchocerca spp., Opisthorchis spp., Paragonimus spp., Naegleria spp., Schistosoma spp., Strongyloides spp., Toxocara spp., Toxoplasma spp., Trichinella spp., Trichomonas spp., and Trichuris spp. In a suitable embodiment the macroparasite is selected from one or more of Entamoeba histolytica, Ascaris lumbricoides, Balantidium coli, Trypanosoma brucei, Trypanosoma cruzi, Clonorchis sinensis, Cyclospora cayetanensis, Taenia solium, Desmodesmus armatus, Dientamoeba fragilis, Dracunculus medinensis, Enterobius vermicularis, Fasciolopsis buski, Giardia lamblia, Necator americanus, Hymenolepis nana, Hymenolepis diminuta, Isospora belli, Wuchereria bancrofti, Rhinosporidium seeberi, Brugia malayi, Plasmodium vivax, Plasmodium falciparum, Plasmodium malariae, Plasmodium ovale, Plasmodium knowlesi Onchocerca volvulus, Opisthorchis viverrini, Opisthorchis felineus, Naegleria fowleri, Strongyloides stercoralis, Toxoplasma gondii, Trichinella spiralis,Trichuris trichiura, and Trichomonas vaginalis. In a suitable embodiment, the infective agent is an antibiotic-resistant bacterium (e.g. MRSA), preferably a multi-antibiotic resistant bacterium. An antibiotic resistant bacterium may be resistant to beta-lactams, such as methicillin. Antibiotic resistance may be assessed using any technique known in the art, such as the Kirby-Baure method, Stokes method, Etest, and / or agar and broth dilution methods for minimum inhibitory concentration (MIC) determination. In a suitable embodiment a bacterial infective agent is resistant to one or more of a penicillin, a penicillinase-resistant penicillin, a cephalosporin, a beta-lactamase inhibitor, a tetracycline and combinations thereof, or pharmaceutically acceptable salts thereof. In a suitable embodiment a bacterial infective agent is resistant to one or more of: vancomycin, nafcillin, oxacillin, teicoplanin, penicillin, methicillin, flucloxacillin, dicloxacillin, cefazolin, cephalothin, cephalexin, cefuroxime, clindamycin, cefazolin, amoxicillin / clavulanate, ampicillin / sulbactam, lincomycin, erythromycin, trimethoprim, sulfamethoxazole, daptomycin, linezolid, rifampin, ciprofloxacin, gentamycin, tetracycline, doxycycline, minocylcine, tigecycline and combinations thereof or pharmaceutically acceptable salts thereof. In a suitable embodiment a bacterium may be resistant to vancomycin and / or teicoplanin, or pharmaceutically acceptable salts thereof. A multi-antibiotic resistant bacterium is resistant to at least 2, 3, 4, 5, 6, 7, 8, 9 or 10 antibiotics (e.g. chemical antibiotics). In a suitable embodiment, cells of a population of cells of the invention, or of a pharmaceutical composition of the invention, or produced on differentiation of such cells kill an infective agent by phagocytosing a cell infected by the infective agent. For example, in a suitable embodiment, a a virus is killed by phagocytosing a cell infected by the virus. In a suitable embodiment, a bacterium is killed by phagocytosing a cell infected by the bacterium. In a suitable embodiment, cells of a population of cells of the invention, or of a pharmaceutical composition of the invention, or produced on differentiation of such cells, kill an infective agent by releasing one or more factors which kill the infective agent. For example, in a virus is killed by release of one or more factors which kill the virus. In a suitable embodiment, a bacterium is killed by release of one or more factors which kill the bacterium. In some embodiments, a population of cells of the invention, or pharmaceutical composition of the invention, or produced on differentiation of such cells, kills an infective agent by a combination of the above. Suitably, a population of cells of the invention, or pharmaceutical composition of the invention, may comprise cells capable of differentiating (preferably that differentiate) to give rise to granulocytes that have cytocidal activity that may further contribute to a therapeutic immune response. In particular, such cells may produce granulocytes that are able to kill cancer cells, infected cells, or cellular infective agents. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention for use in treating an infection. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in the manufacture of a medicament for treating an infection. In one aspect, the invention provides for a method for treating an infection comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention. The infection may be as taught herein. Autoimmune diseases Suitably, a population of cells of the invention, or pharmaceutical composition of the invention, may be used in the prevention or treatment of an autoimmune disease. Autoimmune diseases are characterized by malfunction or dysregulation of the immune system resulting in inflammation and tissue damage. Existing treatments for autoimmune diseases typically involve medications to suppress the abnormal immune response, alleviate symptoms, and prevent further damage to affected tissues and organs. In a suitable embodiment, the autoimmune disease is selected from the group consisting of: rheumatoid arthritis; psoriatic arthritis; lupus erythematosus; scleroderma; type 1 diabetes; multiple sclerosis; Hashimoto's thyroiditis; celiac disease; graves’ disease; Addison’s disease; inflammatory bowel disease (including Crohn's disease and ulcerative colitis); and psoriasis. In one aspect, the invention provides a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention for use in treating an autoimmune disease. In one aspect, the invention provides for the use of a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention in the manufacture of a medicament for treating an autoimmune disease. In one aspect, the invention provides for a method for treating an autoimmune disease comprising administering to a subject in need thereof a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a population of granulocyte precursor cells of the invention or a pharmaceutical composition of the invention. The autoimmune disease may be as taught herein. In one aspect, the invention provides a kit comprising: a) a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a pharmaceutical composition thereof; and / or b) a population of granulocyte precursor cells of the invention as taught herein or a pharmaceutical composition thereof; and c) optionally instructions for use of the same in medicine, e.g. in treating cancer and / or an infection and / or an autoimmune disorder. In one aspect, the invention provides a kit comprising: a) a granulocyte or a granulocyte precursor cell (preferably the granulocyte precursor cells of the invention as taught herein) or a pharmaceutical composition thereof; and / or b) a population of granulocyte precursor cells of the invention as taught herein or a pharmaceutical composition thereof; and c) instructions for use of the same in medicine, e.g. in treating cancer and / or an infection and / or an autoimmune disorder. General considerations Prior to administration there may be a matching step between a population of cells of the invention, or pharmaceutical composition of the invention, and the subject to be treated. Matching may be based on data derived from the donor from which the population of cells of the invention, or pharmaceutical composition of the invention, is derived, and similar data obtained from the subject to be treated. Matching may be achieved on the basis of blood group type, human leukocyte antigen (HLA) type similarity, or combinations thereof. Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this disclosure belongs. Singleton, et al., DICTIONARY OF MICROBIOLOGY AND MOLECULAR BIOLOGY, 20 ED., John Wiley and Sons, New York (1994), and Hale & Marham, THE HARPER COLLINS DICTIONARY OF BIOLOGY, Harper Perennial, NY (1991) provide the skilled person with a general dictionary of many of the terms used in this disclosure. This disclosure is not limited by the exemplary methods and materials disclosed herein, and any methods and materials similar or equivalent to those described herein can be used in the practice or testing of embodiments of this disclosure. Numeric ranges are inclusive of the numbers defining the range. Unless otherwise indicated, any nucleic acid sequences are written left to right in 5' to 3' orientation; amino acid sequences are written left to right in amino to carboxy orientation, respectively. The headings provided herein are not limitations of the various aspects or embodiments of this disclosure. Amino acids are referred to herein using the name of the amino acid, the three letter abbreviation or the single letter abbreviation. The term “protein", as used herein, includes proteins, polypeptides, and peptides. As used herein, the term “amino acid sequence” is synonymous with the term “polypeptide” and / or the term “protein”. In some instances, the term “amino acid sequence” is synonymous with the term “peptide”. In some instances, the term “amino acid sequence” is synonymous with the term “enzyme”. The terms "protein" and "polypeptide" are used interchangeably herein. In the present disclosure and claims, the conventional one-letter and three-letter codes for amino acid residues may be used. The 3- letter code for amino acids as defined in conformity with the IUPACIUB Joint Commission on Biochemical Nomenclature (JCBN). It is also understood that a polypeptide may be coded for by more than one nucleotide sequence due to the degeneracy of the genetic code. Other definitions of terms may appear throughout the specification. Before the exemplary embodiments are described in more detail, it is to be understood that this disclosure is not limited to particular embodiments described, and as such may vary. It is also to be understood that the terminology used herein is for the purpose of describing particular embodiments only, and is not intended to be limiting, since the scope of the present disclosure will be defined only by the appended claims. Where a range of values is provided, it is understood that each intervening value, to the tenth of the unit of the lower limit unless the context clearly dictates otherwise, between the upper and lower limits of that range is also specifically disclosed. Each smaller range between any stated value or intervening value in a stated range and any other stated or intervening value in that stated range is encompassed within this disclosure. The upper and lower limits of these smaller ranges may independently be included or excluded in the range, and each range where either, neither or both limits are included in the smaller ranges is also encompassed within this disclosure, subject to any specifically excluded limit in the stated range. Where the stated range includes one or both of the limits, ranges excluding either or both of those included limits are also included in this disclosure. It must be noted that as used herein and in the appended claims, the singular forms “a”, “an”, and “the” include plural referents unless the context clearly dictates otherwise. Thus, for example, reference to “a population of granulopoietic cells” includes a plurality of such populations and reference to “the population of granulopoietic cell” includes reference to one or more granulopoietic cell populations and equivalents thereof known to those skilled in the art, and so forth. The publications discussed herein are provided solely for their disclosure prior to the filing date of the present application. Nothing herein is to be construed as an admission that such publications constitute prior art to the claims appended hereto.

[0002] EXAMPLES The following examples illustrate certain aspects and embodiments of the invention. EXAMPLE 1: Method for producing a population of granulocytes, or granulocyte precursor cells Without wishing to be bound by theory, the IMANs ((aka the granulocyte and / or precursor cells of the invention) differentiated in vitro (obtainable or obtained by the methods of the invention, e.g. as exemplified in Examples 2-6)) appear to include a number of different cell populations, at least some of which appear to be closest to in vivo differentiated promyelocytes, myelocytes or intermediate cells thereof. Thus, the IMANs, may be considered to be granulocyte precursor cells. The IMANs of the invention are endowed with several advantages including at least the following: High cytocidal activity such as high cancer killing activity: The present inventors have shown that the IMANs of the invention exbibit high cancer killing activity (regardless of cancer type or mutation status) when used alone (monotherapy) as well as when used in combination with another therapeutic agent such as an antibody, a check point inhibitor, a CAR-T cell, etc, (combination therapy). Specifically, IMANs exhibit strong immunomodulatory effects by recruiting and activating effector immune cells, such as T cells and NK cells, etc., within the tumour microenvironment (in vitro, ex vivo, and in vivo) to further enhance anti-cancer efficacy. Additionally, IMANs synergises effectively with antibody therapies (e.g. Cetuximab) by enhancing antibody-dependent cellular cytotoxicity (ADCC) as well as enhancing the effectiveness of immune checkpoint inhibitors (CPIs) (e.g. Nivolumab) and CAR-T cells. Distinct gene marker profile: In addition to the distinct cell surface marker profile described herein, the present inventors have surprisingly found that the IMANs of the invention also exhibits a gene marker profile that is distinct (non-naturally occurring) from that observed in vivo in natural (wild type) cells at the same developmental stage, as well as from cells at the same developmental stage generated in vitro by other methods. Specifically, the IMANs of the invention are associated with increased expression of one or more of: SRGN, MPO, HLA-DRA, CD74, and ELANE; and / or a decreased expression of one or more of: DEFA1, DEFA3, CAMP, BPI, and AZU1, when compared to an equivalent granulocyte precursor cell (e.g. promyelocyte, myelocyte, and / or intermediate cell thereof or any combination thereof) that has been differentiated in vivo. Without wishing to be bound by any theories, it is believed that this unique gene marker profile (in addition to the unique cell surface marker profile described herein) underlies, at least in part, the beneficial attributes associated with IMANs as described herein. These include enhanced functional characteristics such as high cytocidal (e.g. potent cancer-killing) activity, enhanced capacity to recruit and activate effector immune cells like T-cells and NK cells, enhanced potency when used in combination with other therapeutic agents (e.g. antibody, CPI, CAR-T cell), and improved persistence both in vitro and in vivo, characterised by prolonged survival, sustained activity, and continued functional efficacy following administration in vivo to an organism (e.g. mice) or subject. Such unique gene marker profile may also be used as part of a batch release assay for a cell-based therapy. This may be beneficial from a regulatory perspective, as it may provide a robust, specific, and quantifiable method to confirm the identity, purity, and / or consistency of the therapeutic cell product before its release. Such a marker profile may also be beneficial to enhance quality control processes by distinguishing the therapeutic cells from contaminants or undesired cell types and verifying that the cells retain their intended characteristics batch-to-batch. High persistence (survival) both in vitro and in vivo The present inventors showed that the IMANs of the invention exhibit enhanced persistence both in vitro and in vivo. Specifically, the IMANs of the invention demonstrated prolonged survival and sustained activity over time both in in vitro cultures and in vivo following administration in living organisms (e.g. mice model). Such enhanced persistence indicates that the IMANs of the invention are able to maintain viability, proliferate, and exert their therapeutic effects for an extended duration, which is needed for achieving long-lasting clinical benefits. This is important because in vivo persistence is often correlated with improved treatment outcomes, as the therapeutic cells remain effective in the patient’s body, resist exhaustion or clearance, and continue to exert therapeutic benefits (e.g. cancer killing activity). Enhanced persistence is a desired characteristics in cell-based therapies (e.g. IMANs, CAR-T cell, etc), where prolonged activity is linked to sustained remission of the disease being treated (e.g. cancer). Manufacturing process and therapeutic that are free of animal-derived products: The IMANs of the invention may be manufactured under GMP conditions with high scalability and cost-efficiency (as per the methods of the invention), completely free of animal-derived materials (none of the culture media of the invention, e.g. as exemplified Examples 2-6 and in Table 9 contain animal-derived materials). This is important because the use of animal- derived materials (e.g. serums, hormones, and growth factors, etc.) in cell-based therapy manufacturing introduces unwanted risks and challenges. For instance, animal-derived materials may introduce infectious agents, such as viruses or other pathogens, potentially compromising patient safety and contaminating production batches. Additionally, animal- derived components often exhibit batch-to-batch variability that impacts product consistency, quality, and reproducibility, which are factors under strict regulatory scrutiny. Therefore, the culture media and methods of the invention are beneficial as they not only enhance safety but also may facilitate streamlined compliance with regulatory standards. Consequently, the methods and culture medias of the invention result in the production of a therapeutic product (IMANs) that is free of animal-derived products. The methods of the invention all produce IMANs exhibiting one or more of the beneficial characteristics described above; however, it was found that using culture media v0.4d in these methods provides particularly advantageous results. IMANs produced with culture media v0.4d display several or all of the beneficial characteristics more consistently and at higher yields. In other words, methods using culture media v0.4d are especially effective for producing IMANs with the desired beneficial properties. The manufacturing process has been established as follows. After collection of cells from healthy donor leukapheresis, the manufacturing process consists of three main stages: 1. Step 1: Isolation and cryopreservation of CD34+ stem cells (HSCs) from donor leukapheresis. The donors were selected according to the method of Example 1A below. Specifically, CD34+ stem cells (HSCs) were obtained from donor having granulocytes (neutrophils) with high cytocidal activity (e.g. high cancer killing activity) as described herein. 2. Step 2: Expansion of isolated CD34+ stem cells (HSCs) for 9 days (termed “E0” to “E8”) in expansion medium (e.g. as described below in Examples 2-6 and Table 9). This expansion phase generates intermediate progenitor cells (granulocyte progenitor cells) from the CD34+ stem cells (HSCs). At the end of the expansion phase, expansion media is replaced with differentiation media (e.g. as described below in Examples 2-6 and Table 9). 3. Step 3: Differentiation of intermediate / primitive progenitor cells (granulocyte progenitor cells) for 4 or 5 days (termed “D0” to “D5”). The constituents of the differentiation medium used change over time, as described in more detail below (e.g. Examples 2-6 and Table 9). At the end of the differentiation phase a population of cells primarily made up of granulocytes, or granulocyte precursor cells (promyelocyte, myelocyte, and / or intermediate cell thereof or any combination thereof), is produced. These cells (also referred to as IMANs, or IMANps) constitute an active drug substance (DS) for various therapeutic applications. The expansion phase (Step 2) employs cell culture conditions involving cytokine supplementation that may include, or exclude, the addition of interleukins, as discussed further below in Examples 2-6. EXAMPLE 1A: Selection of donors The donors of Example 1 were selected as set out below: Donors were pre-selected based on their ability to produce granulocytes (neutrophils) exhibiting high levels of Cancer Killing Activity (CKA) in a cancer killing activity assay described in Example 1B below. Specifically, a donor was selected if said donor: a. produced granulocytes (neutrophils) that were capable of killing at least 30%, preferably 50% or more preferably at least 70% of the cancer cells (i.e. having at least 30% CKA, 50% CKA or 70% CKA, respectively) in the cancer killing assay as set out in Example 1B); and b. fulfilled the selection criteria in Tables A, B and C: Table A: Inclusion criteria: No prior or concurrent malignancy (either solid tumor or hematological) with the following exceptions: • Adequately treated basal cell or squamous cell carcinoma of the skin • In situ carcinoma of the cervix treated curatively and without evidence of recurrence for at least 12 months prior to screening. Good venous access (has adequate antecubital veins for peripheral access during apheresis). No active infection or history of recurrent infection. Normal liver function: liver function tests acceptable up to 2 x the upper limit of normal. If greater than 2 x the upper limit of normal, is acceptable if a normal liver ultrasound and less than three times the upper limit of normal. Normal blood count: (White blood cells (WBC) 3000 to 10,000 / mm(3), neutrophils greater than 1500 / mm(3), platelets greater than 150,000 / mm(3), haemoglobin greater than 12.5 g / dL for females and 13.5 g / dL for males, Mean Corpuscular Volume (MCV) and Mean Corpuscular Hemoglobin Concentration (MCHC) normal. Normal cardiovascular function, no history of chest pain, myocardial infarction, peripheral vascular disease, transient ischemic attack, or stroke. If a woman, not pregnant or lactating. Must be able to comprehend the investigational nature of the study and provide informed consent to participate in the study. Full HLA typing will be completed for all donors. Table B: Exclusion criteria: > 38 degrees Celsius, or white blood cell (WBC) > 9000 / mm3. Above 50kg but has a body mass index of less than 40. Severe lung disease, such as asthma (other than controlled or childhood resolved), emphysema or lung fibrosis. Uncontrolled high blood pressure (>160 / 100), abnormal heart rhythm or other heart problems. Had a stroke, heart attack, heart failure, angina, heart bypass operation or heart valve replacement. Autoimmune condition (assessed on a case-by-case basis). Receiving treatment for epilepsy or certain other neurological conditions (assessed on a case-by-case basis). Evaluate risk of contracting hepatitis C, HIV, malaria and other infections - for example, through high-risk sexual behaviour, intravenous drug use, travelling in areas of high risk for infectious diseases or tattooing. Anaemia (Haemoglobin <12.5 g / dL for females and <13.5 g / dL for males)*, sickle cell disease or sickle cell trait. Diagnosed with HIV, hepatitis C or Human T cell lymphotropic virus (HTLV), or currently has hepatitis B. Hemophilia. The subject is currently pregnant. The subject has injected him / herself with illegal or non-prescription drugs including body building drugs in recent years. The subject is involved in high-risk sexual practices that may increase risk of exposure to transmissible diseases. The subject has any positive screening test as listed below in Table C. The subject has an allergy to G-CSF or bacterial E. coli products. The subject has had non-steroidal anti-inflammatory drugs (ibuprofen and aspirin) within 5 days of starting protocol (subject is however allowed to take Tylenol or Ibuprofen while on Filgastrim to offset side effects). *To be checked again on procurement day. The decision to go ahead lies with medical team. Table C: Screening tests: Infectious Disease Markers (IDMs) Tests Human Immunodeficiency Virus 1 & 2 (HIV 1 Anti-HIV 1 & 2 Ab HIV PCR (NAT) & 2) Hepatitis B Virus (HBV) • HBsAg hepatitis B surface antigen • Anti-HBc Ab antibody to hepatitis B core antigen (IgG and IgM) • HBV PCR (NAT) Human T-cell Lymphotropic Virus 1 & 2 Anti-HTLV – 1 Ab & Anti-HTLV – 2 Ab (HTLV 1 & 2) Hepatitis C Virus (HCV) • Anti-HCV Ab • HCV PCR (NAT) Syphilis Treponema pallidum antibody test Chagas Anti-T.cruzi Extra tests for both Research Use Only (RUO) and Good Manufacturing Practice (GMP) Leukopaks - * Only Repeat Tests on Day of Collection GMP Leukopaks for EMA Requirements Hepatitis E (HepE) HEV RNA (NAT) Cytomegalovirus (CMV) Anti-CMV (IgG and IgM) - Total CMV (not separated IgG and IgM in standard panel) Zika virus PCR test for Zika Virus West Nile virus (WNV) (WNV NAT) - In Standard Panel Epstein Barr Virus (EBV) Anti-EBV IgG and IgM HIV-1 / HIV-2 Plus O EIA *Required for UK JPAC (Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee) EXAMPLE 1B: Cancer Killing Assay The cancer killing activity of the granulocytes (neutrophils) obtained from healthy donors was assessed using the method described below. Materials and Method: Table D: Materials used Material Supplier Storage condition A549-Luc2 ATCC (American Type ≤ -150 (luciferase-expressing Culture Collection) Cat. No. human lung carcinoma cell CCL-185. line used as target cancer cells) SupT1 ATCC (American Type ≤ -150 (human T-cell lymphoma cell Culture Collection), Cat. No. line used as a biological CRL-1942 assay control) Whole blood (WB) From human donor Ambient (18- 25°C) (peripheral blood from human donor) MACSxpress Whole Blood Miltenyi (Cat. No. 130-104- 2-8°C Neutrophil Isolation Kit 434) (general reagent) Red blood cell lysis solution Miltenyi (Cat. No. 130-094- 2-8°C (10x) 183) (general reagent) Staurosporine General Merck (Cat. No. S6942- ≤ -20°C Reagent 200UL) Assay medium (50 mL) 49.5 mL of DMEM (Life Pre-warm assay media to Technologies / Thermo Fisher 37°C before use and keep at Cat. No.21063029) + 0.5 mL oom temperature while in penicillin / streptomycin (Life use, store at 2-8°C overnight Technologies, Cat. No> and discard any unused 15140122). media at the end of Day 2. Cancer killing assay Step 1 (day 1): The A549-Luc2 cells (referred to herein as “target cells”) were expanded and plated (in triplicate) in a 96 well plates (SLS Cat. No. 353296) and incubated overnight at 37ºC to allow the cells to adhere to the 96 well plate. Step 2 (day 2): Fresh, whole blood (WB) was drawn from donors the next morning (with written consent). The granulocytes were isolated from WB using a neutrophil isolation kit (MACSxpress Whole Blood Neutrophil Isolation Kit), as per manufacturer’s instructions. Granulocytes (neutrophils) were isolated from WB as soon as possible after the blood draw. Specifically, the time elapsed between blood collection from the donor and the start of granulocyte (neutrophil) isolation was less than 12 hours. The purity of the isolated granulocytes (neutrophils) was assessed by flow cytometry for cell surface markers CD15 and CD66b. Both CD15 and CD66b were required at a minimum for acceptance criteria for the samples. The granulocyte (neutrophil) isolation resulted in > 98% of the granulocytes (neutrophils) positive for CD15+ / CD66b+, thereby confirming purity of the granulocyte (neutrophil) sample to be tested in the cancer killing assay. On the same day, the freshy isolated granulocytes (neutrophils) referred to herein as “effector cells” were added to the wells containing the target cells at an effector to target ratio of [10:1], [20:1], and [40:1]. Two separate positive controls were used in the assay and tested in triplicates: 1) a chemical (staurosporine) positive control and 2) a biological positive control (SupT1 cells). The positive controls were added to separate wells of the same 96-well plate containing A549-Luc2 cells as follows: SupT1 was added at an effector to target ratio of [20:1] and [40:1] while staurosporine was added to wells containing A549-Luc2 cells at two concentrations 0.2 µM and 10 µM. Two negative controls were also used and added to separate wells of the same 96-well plate: 1) wells containing the assay medium only, and 2) wells containing A549-Luc2 cells. The 96-well plate was then read (for luminescence signal) after a defined duration of co-incubation (18h) at 37°C / 5% Co2using a luminescence plate reader (GloMax Discover, Promega). Percentage (%) lysis was calculated based on the luminescence reading of the sample wells in comparison to target only (A549-Luc2 cells) wells. The results are shown in Figure 21A and B. Granulocytes (neutrophils) from 17 donors (who met the requirements of Tables A-C) were tested in the cancer killing assay. Out of the 17 donors tested, five (5) donors were identified as being donors producing granulocytes (neutrophils) with high cancer killing activity (CKA). Specifically, said donors were selected because they had granulocytes (neutrophils) that consistently show capacity to kill cancer cells above the mean across all Effector:Target cell ratio tested. Figure 21A shows that granulocytes (neutrophils) from said donors exhibited above 30% lysis at [10:1], above 45% at [20:1], and above 60% at [40:1]. The percentage of lysis observed for the granulocytes (neutrophils) with high CKA was similar or superior to the percentage of lysis observed with the positive controls (known cytotoxic agents) SupT1 and staurosporine (Figure 212B), thus confirming the robust (high) CKA of the granulocytes (neutrophils) tested. Table E shows a representative example of the percentage (%) lysis observed with IMANs derived from donors whose granulocytes (neutrophils) exhibit high cancer killing activity as selected by the method described above. IMANs exhibit percentage (%) of lysis that is comparable to or exceed those of well-established cytotoxic agents used as positive controls, namely SupT1 cells and staurosporine. Table E IMANs (n=3) SupT1 SupT1 Staurosporine Staurosporine [40:1] [20:1] [40:1] [0.2 µM] [10 µM] % Lysis 70 65 85 30 95

[0003] EXAMPLES 2 TO 6: Specific embodiments of the methods of preparing granulocytes, or granulocyte precursor cells, for therapeutic use Examples 2 to 6 set out different embodiments of methods of the invention for preparing cells for therapeutic use. The methods are based on culture of stem cells (e.g. HCS) as starting material, and result in the production of granulocytes, or granulocyte precursor cells (e.g. a promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). The methods involve supplementation with stem cell factor (SCF), FLT3 ligand (FLT3-L) and thrombopoietin (TPO) during the expansion phase. The expansion phase may also incorporate supplementation with interleukins, particularly IL-3 and IL-6, (methods designated v0.4c) or may lack interleukin supplementation (methods designated v0.4d). The methods may employ UM729 or UM171 as examples of a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells. The culture media and their respective components, including specified quantities, used in methods v0.4c and v0.4d, as well as the culture media for method v0.3c, are detailed in Table 9. Examples 2-6 illustrate practical applications of these culture media for producing the cells of the invention (IMANs). EXAMPLE 2: Method for producing a population of granulocytes, or granulocyte precursor cells, using interleukin supplementation and UM729 (“v0.4c” protocol with UM729) At E0, CD34+ HSCs were thawed in thaw medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with human serum albumin (HSA) at 1% w / v concentration; and centrifuged at 300G for 5 mins. Cells were then resuspended in expansion base medium (IMDM with glutamax or L- glutamine, 1 X ITS, 1% HSA) and the concentration was adjusted to 5E5 cells / ml (the skilled person understands that this is equivalent to 5 x 105cells). The following cytokines - SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml), IL-3 (0.015 µg / ml), and IL-6 (0.015 µg / ml) - were then added to the cell suspension. All cytokines are reconstituted to a stock solution of 100 µg / ml as per manufacturer’s recommendations. 10 ml of the cell suspension was seeded into one well of G-REX 6M to achieve 5E5 cells / cm2. The following day, E1, cells were resuspended. A sample of the resuspended cells were counted, the cell viability was assessed, and flow cytometry was used for characterisation. On E1, the cells were fed with 30 ml of expansion medium (expansion base medium supplemented with SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml), IL-3 (0.015 µg / ml), and IL-6 (0.015 µg / ml)) to top up the total volume to 40 ml. Then, 4 µL of a 5 mM stock solution of UM729, a pyrimido-[4,5-b]-indole derivative, was added to the well, to produce an overall concentration of 500 nM in the expansion media. Cells remained in the above medium for days E2 and E3 of the expansion phase. On E4, cells were resuspended, with a sample taken for a cell count and for flow cytometry. Cells were seeded in a new well plate into fresh expansion medium at a seeding density of 1E5 cells / cm2and a media volume of 50 ml. The UM729 concentration was set at 500 nM, equating to 5 µl of 5 mM stock solution added to the well. Cells remained in the above medium for E5. On E6, cells were resuspended, with a sample taken for a cell count and for flow cytometry. 50 ml of expansion media was added to the wells to a total volume of 100 ml. The UM729 concentration was set at 1uM, equating to 20 µl of 5 mM stock solution added to the well. The last day of the expansion phase (E8) is the point at which the expansion medium is changed to differentiation medium and the differentiation commences (D0). This timepoint is referred to as E8D0. Of the 100 ml of total media volume from E6, at E8D0, 40 ml of medium is transferred from the well to a sterile tube, while the remaining 60 ml is aspirated to 10 ml or less without disturbing the cell layer. Resuspension of the cells is achieved by swirling. A cell suspension was then prepared at a concentration of 0.5-2E6 cells / cm2, 10 ml of which was added to each new well, giving rise to 5E6 – 20E6 cells seeded per well overall. An additional 40 ml of media was required to reach a total volume of 50 ml of media. For the cytokine supplementation, 0.333 ng of cytokine (SCF, TPO, and G-CSF) was added to the well per 1E3 cells seeded. Where 1E6 cells / cm2was the target seeding density for a 10 cm2area, 10E6 cells were seeded overall. Accordingly, 3.33 µg of cytokine was provided in the 40 ml of media added to top up the well to a total volume of 50 ml. Therefore, at a seeding density of 1E6 cells / cm2, 0.083 µg / ml of each cytokine was added to the well. Importantly, this concentration is of the media that is added to the well. Cells remained in the above medium for E8D1. On E8D2, the cells were resuspended and a sample was taken for cell count and flow cytometry analysis. At this stage, 50 ml of fresh media was added, supplemented with cytokines SCF, TPO, and G-CSF at an amount double that provided on E8D0 (0.666 ng of cytokine per 1E3 cells seeded). Therefore, the concentration of each cytokine was 0.166 µg / ml for SCF, TPO, and G-CSF. Furthermore, at E8D2, GM-CSF (0.01 µg / ml) and IL-3 (0.130 µg / ml) were also added to the media. On E8D3, the only addition made to the medium is TNFα to produce a final concentration of 0.001 µg / ml. On E8D4, 75 ml of medium was removed from each well. The cells in the well were resuspended in the remaining medium by gentle pipetting. A sample was taken for cell count and flow cytometry. The remaining 25 ml of cell suspension was centrifuged at 300 G for 5 minutes. On the formation of the cell pellet, the cells were resuspended in cold CS10 aliquots and into cryotubes. The cells generated by this method comprise granulocyte precursor cells granulocyte precursor cells (e.g. promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). Cells were frozen at a concentration around 10 x 106viable cells / vial. EXAMPLE 3: Method for producing a population of granulocytes, or granulocyte precursor cells, using UM729 without interleukins (“v0.4d” with UM729) At E0, CD34+ HSCs were thawed in thaw medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with HSA at 1% w / v concentration; and centrifuged at 300G for 5 mins. Cells were then resuspended in expansion base medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with glutamax or L-glutamine, 1 X ITS, and 1% HSA; and the concentration was adjusted to 5x105cells / ml. The following cytokines - SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml) – were then added to the cell suspension. All cytokines are reconstituted to a stock solution of 100 µg / ml as per manufacturer’s recommendations. 10 ml of the cell suspension was seeded into one well of G-REX 6M to achieve 5E5 cells / cm2. The following day, E1, cells were resuspended. A sample of the resuspended cells were counted, the cell viability was assessed, and flow cytometry was used for characterisation. The cells were fed with 30 ml of expansion medium – expansion base medium supplemented with SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml) - to top up the total volume to 40 ml. Then, 4 µL of a pyrimido-[4,5-b]-indole derivative, UM729, at a concentration of 5 mM stock solution was added to the well, to produce an overall concentration of 500 nM in the expansion media. Cells remained in the above medium for E2 and E3. On E4, cells were resuspended, with a sample taken for a cell count and for flow cytometry. Cells were seeded in a new well plate into fresh expansion medium at a seeding density of 1E5 cells / cm2and a media volume of 50 ml. The UM729 concentration was set at 500 nM, equating to 5 µl of 5 mM stock solution added to the well. Cells remained in the above medium for E5. On E6, cells were resuspended, with a sample taken for a cell count and for flow cytometry. 50 ml of expansion media was added to the wells to a total volume of 100 ml. The UM729 concentration was set at 1 µM, equating to 20µl of 5 mM stock solution added to the well. The last day of expansion (E8) is the point at which the expansion is changed to differentiation medium and the differentiation commences (D0). This timepoint is referred to as E8D0. Of the 100 ml of total media volume from E6, at E8D0, 40 ml of medium is transferred from the well to a sterile tube, then aspirated to 10 ml or less without disturbing the cell layer. Resuspension of the cells is achieved by swirling. “Measure the volume remaining and take a sample for cell count, viability, and flow cytometry.” A cell suspension was then prepared at a concentration of 1x106cells / ml, 10 mls of which was added to each new well, giving rise to 10x106cells seeded per well overall. An additional 40 ml of media was required to reach 50 ml of media overall. For the cytokine supplementation, 0.333 ng of cytokine (SCF, TPO, and G-CSF) was added to the well per 1E3 cells seeded. Where 1E6 cells / cm2was the target seeding density for a 10 cm2area, 10E6 cells were seeded overall. Accordingly, 3.33 µg of cytokine was provided in the 40 ml of media added to top up the well to a total volume of 50 ml. Therefore, at a seeding density of 1E6 cells / cm2, 0.083 µg / ml of each cytokine was added to the well. Importantly, this concentration is of the media that is added to the well. Cells remained in the above medium for E8D1. On E8D2, the cells were resuspended and a sample was taken for cell count and flow cytometry analysis. At this stage, 50 ml of fresh media was added, supplemented with cytokines SCF, TPO, and G-CSF at an amount double that provided on E8D0 (0.666 ng of cytokine per 1E3 cells seeded). Therefore, the concentration of each cytokine was 0.166 µg / ml for SCF, TPO, and G-CSF. Furthermore, at E8D2, GM-CSF (0.01 µg / ml) and IL-3 (0.130 µg / ml) were also added to the media. On E8D3, the only addition made to the medium is TNFα to produce a final concentration of 0.001 µg / ml. On E8D4, 75 ml of medium was removed from each well. The cells in the well were resuspended in the remaining medium by gentle pipetting. A sample was taken for cell count and flow cytometry. The remaining 25 ml of cell suspension was centrifuged at 300 G for 5 minutes. On the formation of the cell pellet, the cells were resuspended in cold aliquots and into cryotubes. The cells generated by this method comprise granulocyte precursor cells granulocyte precursor cells (e.g. promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). Cells were frozen at a concentration around 10 x 106viable cells / vial. The cells were characterised repeatedly throughout the expansion and differentiation phases using flow cytometry. EXAMPLE 4: Method for producing a population of granulocytes, or granulocyte precursor cells, using UM171 and interleukins (“0.4c” with UM171) At E0, CD34+ HSCs were thawed in thaw medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with human serum albumen (HSA) at 1% w / v concentration; and centrifuged at 300G for 5 mins. Cells were then resuspended in expansion base medium (IMDM with glutamax or L- glutamine, 1 X ITS, and 1% HSA) and the concentration was adjusted to 5E5 cells / ml. The following cytokines - SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml), IL-3 (0.015 µg / ml), and IL-6 (0.015 µg / ml) - were then added to the cell suspension. All cytokines are reconstituted to a stock solution of 100 µg / ml as per manufacturer’s recommendations. 10 ml of the cell suspension was seeded into one well of G-REX 6M to achieve 5E5 cells / cm2. The following day, E1, cells were resuspended. A sample of the resuspended cells were counted, the cell viability was assessed, and flow cytometry was used for characterisation. The cells were fed with 30 ml of expansion medium to top up the total volume to 40 ml. Then, 4 µL of a pyrimido-[4,5-b]-indole derivative, UM171, at a concentration of 1mM stock solution was added to the well, to produce an overall concentration of 50nM in the expansion media. Cells remained in the above medium for E2 and E3. On E4, cells were resuspended, with a sample taken for a cell count and for flow cytometry. Cells were seeded in a new well plate into fresh expansion medium at a seeding density of 1E5 cells / cm2and a media volume of 50 ml. The UM171 concentration was set at 25 nM, equating to 1.25 µl of 1 mM stock solution added to the well. Cells remained in the above medium for E5. On E6, cells were resuspended, with a sample taken for a cell count and for flow cytometry. 50 ml of expansion media was added to the wells to a total volume of 100 ml. The UM171 concentration was set at 50 nM, equating to 5 µl of 1 mM stock solution added to the well. The last day of expansion (E8) is the point at which the expansion is changed to differentiation medium and the differentiation commences (D0). This timepoint is referred to as E8D0. Of the 100 ml of total media volume from E6, at E8D0, 40 ml of medium is transferred from the well to a sterile tube, then aspirated to 10 ml or less without disturbing the cell layer. Resuspension of the cells is achieved by swirling. “Measure the volume remaining and take a sample for cell count, viability, and flow cytometry.” A cell suspension was then prepared at a concentration of 1x106cells / ml, 10 mls of which was added to each new well, giving rise to 10x106cells seeded per well overall. An additional 40 ml of media was required to reach 50 ml of media overall. For the cytokine supplementation, 0.333 ng of cytokine (SCF, TPO, and G-CSF) was added to the well per 1E3 cells seeded. Where 1E6 cells / cm2was the target seeding density for a 10 cm2area, 10E6 cells were seeded overall. Accordingly, 3.33 µg of cytokine was provided in the 40 ml of media added to top up the well to a total volume of 50 ml. Therefore, at a seeding density of 1E6 cells / cm2, 0.083 µg / ml of each cytokine was added to the well. Importantly, this concentration is of the media that is added to the well. Cells remained in the above medium for E8D1. On E8D2, the cells were resuspended and a sample was taken for cell count and flow cytometry analysis. At this stage, 50 ml of fresh media was added, supplemented with cytokines SCF, TPO, and G-CSF at an amount double that provided on E8D0 (0.666 ng of cytokine per 1E3 cells seeded). Therefore, the concentration of each cytokine was 0.166 µg / ml for SCF, TPO, and G-CSF. Furthermore, at E8D2, GM-CSF (0.01 µg / ml) and IL-3 (0.130 µg / ml) were also added to the media. On E8D3, the only addition made to the medium is TNFα to produce a final concentration of 0.001 µg / ml. On E8D4, 75 ml of medium was removed from each well. The cells in the well were resuspended in the remaining medium by gentle pipetting. A sample was taken for cell count and flow cytometry. The remaining 25 ml of cell suspension was centrifuged at 300 G for 5 minutes. On the formation of the cell pellet, the cells were resuspended in cold aliquots and into cryotubes. The cells generated by this method comprise granulocyte precursor cells granulocyte precursor cells (e.g. promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). Cells were frozen at a concentration around 10 x 106viable cells / vial. EXAMPLE 5: Method for producing a population of granulocytes, or granulocyte precursor cells, using UM171 without interleukins (“v0.4d” with UM171) At E0, CD34+ HSCs were thawed in thaw medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with HSA at 1% w / v concentration; and centrifuged at 300G for 5 mins. Cells were then resuspended in expansion base medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with glutamax or L-glutamine, 1 X ITS, and 1% HSA; and the concentration was adjusted to 5E5 cells / ml. The following cytokines - SCF (0.2 µg / ml), FLT- 3L (0.2 µg / ml), TPO (0.02 µg / ml) – were then added to the cell suspension. All cytokines are reconstituted to a stock solution of 100 µg / ml as per manufacturer’s recommendations. 10 ml of the cell suspension was seeded into one well of G-REX 6M to achieve 5E5 cells / cm2. The following day, E1, cells were resuspended. A sample of the resuspended cells were counted, the cell viability was assessed, and flow cytometry was used for characterisation. The cells were fed with 30 ml of expansion medium – expansion base medium supplemented with SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml) - to top up the total volume to 40 ml. Then, 4 µL of a pyrimido-[4,5-b]-indole derivative, UM171, at a concentration of 1 mM stock solution was added to the well, to produce an overall concentration of 50 nM in the expansion media. Cells remained in the above medium for E2 and E3. On E4, cells were resuspended, with a sample taken for a cell count and for flow cytometry. Cells were seeded in a new well plate into fresh expansion medium at a seeding density of 1E5 cells / cm2and a media volume of 50 ml. The UM171 concentration was set at 25 nM, equating to 1.25 µl of 1 mM stock solution added to the well. Cells remained in the above medium for E5. On E6, cells were resuspended, with a sample taken for a cell count and for flow cytometry. 50 ml of expansion media was added to the wells to a total volume of 100 ml. The UM171 concentration was set at 50 nM, equating to 5 µl of 1 mM stock solution added to the well. The last day of expansion (E8) is the point at which the expansion is changed to differentiation medium and the differentiation commences (D0). This timepoint is referred to as E8D0. Of the 100 ml of total media volume from E6, at E8D0, 40 ml of medium is transferred from the well to a sterile tube, then aspirated to 10 ml or less without disturbing the cell layer. Resuspension of the cells is achieved by swirling. “Measure the volume remaining and take a sample for cell count, viability, and flow cytometry.” A cell suspension was then prepared at a concentration of 1x106cells / ml, 10 mls of which was added to each new well, giving rise to 10x106cells seeded per well overall. An additional 40 ml of media was required to reach 50 ml of media overall. For the cytokine supplementation, 0.333 ng of cytokine (SCF, TPO, and G-CSF) was added to the well per 1E3 cells seeded. Where 1E6 cells / cm2was the target seeding density for a 10 cm2area, 10E6 cells were seeded overall. Accordingly, 3.33 µg of cytokine was provided in the 40 ml of media added to top up the well to a total volume of 50 ml. Therefore, at a seeding density of 1E6 cells / cm2, 0.083 µg / ml of each cytokine was added to the well. Importantly, this concentration is of the media that is added to the well. Cells remained in the above medium for E8D1. On E8D2, the cells were resuspended and a sample was taken for cell count and flow cytometry analysis. At this stage, 50 ml of fresh media was added, supplemented with cytokines SCF, TPO, and G-CSF at an amount double that provided on E8D0 (0.666 ng of cytokine per 1E3 cells seeded). Therefore, the concentration of each cytokine was 0.166 µg / ml for SCF, TPO, and G-CSF. Furthermore, at E8D2, GM-CSF (0.01 µg / ml) and IL-3 (0.130 µg / ml) were also added to the media. On E8D3, the only addition made to the medium is TNFα to produce a final concentration of 0.001 µg / ml. On E8D4, 75 ml of medium was removed from each well. The cells in the well were resuspended in the remaining medium by gentle pipetting. A sample was taken for cell count and flow cytometry. The remaining 25 ml of cell suspension was centrifuged at 300 G for 5 minutes. On the formation of the cell pellet, the cells were resuspended in cold aliquots and into cryotubes. The cells generated by this method comprise granulocyte precursor cells granulocyte precursor cells (e.g. promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). Cells were frozen at a concentration around 10 x 106viable cells / vial. The cells were characterised repeatedly throughout the expansion and differentiation phases using flow cytometry. EXAMPLE 6: Method for producing a granulopoietic cell population with UM171 and without interleukins, at 1L scale (v0.4d with UM171) On E0, the CD34+ HSCs in thaw medium containing Iscove’s Modified Dulbecco’s Medium (IMDM) with HSA at 1% w / v concentration; were centrifuged at 300G for 5 minutes at room temperature. The supernatant above was removed, with 100-200 µL left above the cell pellet into which the cells were resuspended. Additional expansion media - expansion base medium supplemented with SCF (0.2 µg / ml), FLT-3L (0.2 µg / ml), TPO (0.02 µg / ml)) was added to achieve a cell suspension at a concentration of 5E5 viable cells / ml. Thereafter, 10 ml of cell suspension was added to each well of G-Rex 6M to achieve 5E5 cells / cm2. A minimum of 5x106cells was required per well. The well plate was then transferred into an incubator at 37°C and 5% CO2. On E1, cells were resuspended, and a cell count and phenotyping were performed. A volume of 30 ml of expansion medium was pre-warmed for each well, to which 4 µL of 1 mM of UM171 stock solution was added, producing a final concentration of 50 nM. The expansion medium supplemented with UM171 was then added to the cell suspension in each well. The well plate was then transferred to the incubator at 37°C and 5% CO2. Cells remained in the above culture conditions for both E2 and E3. On E4, the culture was scaled up from G-Rex 6M to G-Rex 100M. A minimum of 10x106 cells were required to be seeded and the minimum media volume was 500 ml. From the G-Rex 6M, which contained 40 ml of media, 25 ml was removed without the cell layer being disturbed. Cells were then resuspended in the remaining 15 ml. A sample was taken for the cell count and phenotyping. The cells were then reconstituted in expansion media to a concentration of 2x104cells / ml. A volume of 485 ml of fresh expansion media was added to the 15 ml cell suspension, and the 500 ml was then added to a G-Rex 100M. Then, 25 µL of 500 µM UM171 solution was added to form a final concentration of 25 nM. The UM171 solution was dispersed by swirling the G-Rex 100M or by pipetting. The G-Rex 100M was transferred to an incubator at 37°C and 5% CO2. Cells remained in the above conditions on E5. On E6, cells were resuspended and a sample was taken for a cell count and for phenotyping. A volume of 500 ml of fresh expansion medium was added to the G-Rex 100M, to create a final total volume of 1L. Then, a 100 µL volume of 500 µM UM171 stock solution was added to the G-Rex 100M, producing a final concentration of 50 nM. The UM171 was dispersed by swirling the G-Rex 100M or by pipetting. The G-Rex 100M was transferred to an incubator at 37°C and 5% CO2. Cells remained in the above conditions on E7. On E8D0, the volume in the G-Rex 100M was reduced from 1L to 120 ml without the cell layer being disturbed. 100 ml of the removed media was retained for a future dilution step should the cell density be over 1x106cells / cm2. The target cell density was therefore 5E5 – 1E6 cells / cm2. Cells were resuspended in the remaining 120 ml volume by swirling the G- Rex 100M container or by pipetting. A sample of cell suspension was taken for cell count and phenotyping. The cell density was calculated in cells / cm2, wherein the G-Rex 100M area for cell growth is 100 cm2. If above the maximum target cell density of 1x106cells / cm2, cells were removed from the 120 ml suspension and diluted accordingly to this value with the previously retained media. Thereafter, 380 ml of fresh differentiation medium was added to the G-Rex 100M. For the cytokine supplementation, 0.333 ng of cytokine (SCF, TPO, and G-CSF) was added to the well per 1E3 cells seeded. Where 1E6 cells / cm2was the target seeding density for a 100 cm2area, 100E6 cells were seeded overall. Accordingly, 33.3 µg of cytokine was provided in the 380 ml of media added to top up the well to a total volume of 500 ml. Therefore, at a seeding density of 1E6 cells / cm2, 0.088 µg / ml of each cytokine was added to the well. Importantly, this concentration is of the media that is added to the well. Cells remained in the above medium for E8D1. On E8D2, the cells were resuspended and a sample was taken for cell count and flow cytometry analysis. At this stage, 500 ml of fresh media was added, supplemented with cytokines SCF, TPO, and G-CSF at an amount double that provided on E8D0 (0.666 ng of cytokine per 1E3 cells seeded). Therefore, the concentration of each cytokine was 0.133 µg / ml for SCF, TPO, and G-CSF. Additionally, 50 µL of 100 µg / ml stock solution of GM-CSF was added to the media, as was 650 µL of 100 µg / ml stock solution of IL-3. The G-Rex 100M was then transferred to the incubator at 37°C and 5% CO2. On E8D3, 10 µL of 100 µg / ml stock solution of TNFα was diluted in 990 µL of Stemline II media. This TNFα solution was then added to the G-Rex 100M. The G-Rex 100M was then transferred to the incubator at 37°C and 5% CO2. On E8D4, a volume of 900 ml of media was removed, without the cell layer being disturbed. The cells were resuspended in the remaining 100 ml by gentle swirling or by pipetting. A sample was taken to perform a cell count and phenotyping. The suspended cells were transferred into sterile 50 ml centrifuge tubes and centrifuged at 300G for 5 minutes. The supernatant was removed and the cells were resuspended in CS10 to achieve the desired cryopreservation concentration of 40E6 cells / ml. The cells generated by this method comprise granulocyte precursor cells granulocyte precursor cells (e.g. promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof). The cell suspension was then pipetted into cryovials and frozen at -150°C. EXAMPLES 7 TO 15: Investigation of the properties of the granulocytes, or granulocytic precursor cells, produced by the methods of the invention Further studies were undertaken to investigate the properties of the methods of the invention, the properties of the cells produced by these methods of the invention, and the ways in which features of the methods of the invention impact upon the properties of the cells that they produce. As part of these studies, cells produced by methods in accordance with the present invention were assessed with both “reference cells” manufactured by a method (designated “v0.1” internal non-GMP protocol (unpublished), or ABS, which is devoid of a pyrimido-[4,5b]-indole derivative such as UM729 or UM171) that employs animal-derived products, and so is not compatible with production of cells for therapeutic use), or with “comparator cells” cells” which are granulocytes or precursors thereof (granulocyte precursors cells comprising promyelocytes, myelocytes and / or intermediate cells thereof or any combination thereof) produced by a different method which did not use the agent that enhances “stemness” (did not use a pyrimido-[4,5b]-indole derivative such as UM729 or UM171) during cell expansion that was used in the methods of Example 7. EXAMPLE 7: Granulocytic cells produced by methods of the invention demonstrate enhanced cancer cell killing activity compared to comparator cells Cancer killing activity was investigated in a cytotoxicity assay in which granulocytic cells (either produced by the methods of the invention using UM729 with or without interleukin supplementation, e.g. in Examples 2 and 3) or comparator cells (produced according to method v0.3c, Table 9) were cultured with cells of a cancer cell line. In particular, the granulocytic cells were incubated with cells of the human non-small cell lung cancer cell line A549. The A549 cells genetically modified with Luc2 and GFP vector ‘in house’ produced high variability between studies. Therefore, the more reliable cancer cell was A549 EPC, which was commercially available. Granulocytic cells (IMANs) were incubated at an effector:target ratio of 20:1 or 40:1 with the A549 cells that had been further transduced with Luciferase 2 (Luc2). The reduction in the numbers of viable A549-Luc2 cells was calculated, to determine the percentage of A549 cell lysis (%lysis). This allowed quantification of the cancer killing activity of the granulocytic cells. The results are set out in Figure 1. In these bar charts the first two bars (left to right) are respectively granulocytic cells produced by methods of the invention with and without interleukin supplementation in the expansion phase (0.4c and 0.4d protocols). The third bar (if present) represents comparator cells. As can be seen in Figure 1, cells produced by the methods of the invention lysed a higher percentage of cancer cells in each study undertaken. In the case of the “in house” cells, cells produced by the methods of the invention achieved cancer killing activity in the range of approximately 20% to 30%, two to three-fold higher than the 10% lysis achieved by cells produced by previous methods. In the case of the End of Production Cells (A549 EPC), the granulocytic cells of the invention and those produced by previous means each demonstrated cancer killing activity of approximately 10% when tested at a 20:1 effector:target ratio. In contrast, at an effector:target ratio of 40:1 granulocytic cells produced by the methods of the invention showed a marked improvement in cancer killing, achieving cancer killing activity of approximately 40% to 60%, a rate two to three-fold higher than the approximately 20% rate exhibited by the comparator cells. In a further experiment, the present inventors compared the cancer killing activity (ability to lyse A549 cells in vitro) of IMANs produced by the method according to Example 6 in comparison with the granulocyte precursor cells (comparator cells) obtained by a method using culture medium v0.3c (Table 9). The same donors (Donors 1, 2, and 3) were employed for the provision of HSCs used as start material in the method using culture medium v0.04d (as in Example 6) as well as in the method using culture medium v.03c (Table 9) to produce comparator cells. The results are reported in Figure 1A. Specifically, the results show that granulocyte precursors cells (IMANs) differentiated in vitro from HSCs derived from donor with granulocytes (neutrophils) with high cancer killing activity (as assesed per the method of Example 1B) exhibit greater cancer killing activity than granulocyte precursor cells (comparator cells) obtained by a method using culture medium v0.3c (Table 9). The results are shown in fold changes versus v.03c comparator cells. This improvement in cancer cell killing activity that can be achieved by cells produced using the methods of the invention represents an important advance over the previous comparator cells. It is a surprising finding that adding an agent (a pyrimido-[4,5b]-indole derivative such as UM729 or UM171) that enhances “stemness” during cell expansion leads to higher cancer killing activity, which may otherwise be hypothesised to be a function of improved differentiation. EXAMPLE 8: Granulocytic cells produced by the methods of the invention do not adversely impact immune cells in co-culture, and persist in greater numbers than comparator cells The inventors have shown that granulocytic IMAN cells exert immunomodulatory effects that contribute to therapeutic activity. A study was undertaken to compare the impact on immune cells in co-culture of granulocytic cells prepared by the various embodiments of the methods of the invention (using UM729 with or without interleukin supplementation as per the methods as taught in Examples 2 and 3)) and comparator cells. Healthy peripheral blood mononucleocytes (PBMCs) were co-cultured with thawed granulocytic cells (IMANs) prepared either in accordance with an embodiment of the invention (as per the methods of Examples 2-6), or by previous methods (which did not use a a pyrimido-[4,5b]-indole derivative such as UM729 or UM171, referred to as “v0.3c”. The culture medium constituents and specific amounts for the v0.3c method are shown in Table 9). The number of cells present in the culture, and numbers of particular populations of cells within these, were assessed after 48 hours of co-culture. The results are set out in Figure 2. Here it can be seen that the total number of PBMCs remaining in culture did not vary significantly on the basis of the nature of the granulocytic cells used. Similarly, the nature of the granulocytic cells did not significantly impact the numbers of T cells (CD3+ cells) or natural killer (NK) cells present. Accordingly, granulocytic cells (IMANs) produced by the methods of the invention are expected to retain the same immunomodulatory efficacy. When the number of granulocytic cells present at the end of the co-culture period was assessed (results in the graph setting out “granulocytic cells / ml” in Figure 2), it was found that cells (IMANs) manufactured in accordance with any of the embodiments of the methods of the invention investigated remained in culture at higher levels than the comparator cells (generated via the v0.3c method). EXAMPLE 9: Granulocytic cells produced by the methods of the invention exhibit increased persistence in vitro compared to comparator cells The inventors investigated the ability of granulocytic cells (IMANs) produced by the methods of the invention (produced using UM729 without interleukin supplementation as per the method of Example 3) to persist in vitro, with or without supplementation with the cytokine G- CSF. The results of this study are set out in Figure 3, which compares viability and counts in respect of such cells. On day 0 of the study, granulocytic cells were thawed from all conditions in medium comprising IMDM with 2% HSA and ITS. Cells were centrifuged at 300g for 5 mins, then resuspended in IMDM with 2% HSA and ITS. The concentration of cells was adjusted to 1E6 cells / ml, then 4ml of the cell suspension was seeded into 1 well of a G-rex 24. Where applicable, the media was supplemented with G-CSF at 50 ng / ml. On days 1, 2, and 3, the cells were resuspended, the volume was measured, and a sample was taken for cell count and flow cytometry. The total well volume was topped up with a further 4 ml and supplemented with G-CSF, where applicable, at 50 ng / ml to reach a total well volume of 8 ml. As can be seen in Figure 3, cells produced by the methods of the invention (“v0.4d”) persisted to for longer than comparator cells, and for nearly as long as reference cells produced using the non-therapeutically compatible v0.1 protocol (“v0.1”), which was devoid of a pyrimido-[4,5b]-indole derivative such as UM729 or UM171. Both the cells produced in accordance with the methods of the invention and reference cells exhibited an increase of approximately 25% in terms of cell count during the first 24 hours of culture. This was observed with or without supplementation using G-CSF. Viability of the cells produced in accordance with the methods of the invention and of the reference cells are also both higher than the viability of the comparator cells, particularly over the first 7 days of in vitro culture. Viability and cell counts are both increased in respect of all cell types assessed by culture of the cells in the presence of G-CSF. The inventors believe (without wishing to be bound by any theories) that the use of a pyrimido-[4,5-b]-indole derivative (e.g. UM729 or UM171) that promotes the expansion of hematopoietic stem cells in the methods of the invention contributes to the observed increase in persistence. Furthermore, they believe (without wishing to be bound by any theories) that the selection of the pyrimido-[4,5-b]-indole derivative may also influence the extent of persistence. In this regard, use of the pyrimido-[4,5-b]-indole derivative UM171 increases persistence to a greater extent than does UM729. EXAMPLE 10: Granulocytic cells produced by the methods of the invention exhibit enhanced expression of markers associated with commitment to neutrophil lineage, as compared to comparator cells The inventors investigated the markers expressed by granulocytic cells (IMANs) produced by the methods of the invention (produced using UM729 without interleukin supplementation as per the method of Example 3) over time spent in in vitro culture (with or without supplementation with the cytokine G-CSF). Marker expression was compared with reference cells (“v0.1”) and comparator cells (“v0.3c”), both devoid of a pyrimido-[4,5b]-indole derivative such as UM729 or UM171. Marker expression characteristic of four cell profiles was investigated as follows: • Myeloid committed cells: CD15+ • Lineage (“Lin”) committed cells: CD15-; CD11b+; HLA-DR- • Progenitor cells: CD15-; CD11b-; HLA-DR+ • “Off target” differentiation: CD15-; CD11bHi; HLA-DRHi The results of this study are set out in Figure 4, which sets out the proportion of each of the cell types investigated exhibiting markers of the recited cell profiles. As can be seen from Figure 4, expression of CD15 (indicating that the cells are myeloid committed, consistent with the granulocytic cells, or granulocytic precursor cells, being neutrophils, or neutrophil precursors) was highest in the cells of the invention. The cells of the invention (IMANS) express CD15 to a greater extent, and more rapidly, than do the reference or comparator cells. This suggests that the cells (IMANS) of the invention favour commitment to the myeloid (neutrophil) lineage immediately post-thawing, indicating that they are particularly suitable for use in any context for example as such in which it is desired to provide cells capable of differentiating to provide neutrophil activity (for example in the treatment of cancer, or the treatment of infections), than either the reference or comparator cells. The results indicated that each of the groups of cells (cells of the invention IMANs, reference, and comparator) demonstrated a progression from “progenitor” cell marker profile to “lineage committed” cell marker profile with time. However, only the cells of the invention (IMANS) and reference cells appeared to be sustained by this population. None of the methods investigated generated significant populations of “off target” cells, though the proportion of these cells was highest among the comparator cells (produced by a method using v0.3c culture medium, Table 9). EXAMPLE 11: Granulocytic cells prepared in accordance with the methods of the invention contain increased effector granule content as compared to comparator cells Effector granules of granulocytic cells are responsible for many of the cells’ biological activities that make them suitable for therapeutic use. The inventors investigated the expression of the granule constituents neutrophil elastase, myeloperoxidase (MPO), and cathepsin G in cells of the invention (IMANs) (produced using UM729 without interleukin supplementation according to the method of Example 3)), reference cells, and comparator cells (each cultured with or without supplementation with the cytokine G-CSF). The results of this study are shown in Figure 5. Here it can be seen that the cells of the invention (IMANs) co-express neutrophil elastase and MPO more rapidly and to a greater extent (particularly at earlier timepoints) than do the reference or comparator cells. Neutrophil elastase is found within neutrophil-specific granules, and so these results are consistent with those set out in Example 9. Supplementation with G-CSF increases expression of both neutrophil peroxidase and MPO in each of the cell types tested. The ability of the methods of the invention to produce cells (IMANs) with increased effector granule content, and which demonstrate this increased content in the period immediately following cell thawing, demonstrates a marked advantage in the preparation of cells for therapeutic use. It is known that both neutrophil elastase and MPO are able to contribute to anti-tumour activity, and to the ability of granulocytes to fight infections. Accordingly, increasing the extent of these molecules present may be expected to improve therapeutic effectiveness of the cells. Since cell therapies are generally administered to a subject immediately after thawing, the rapid early increase in expression is consistent with the time when such therapeutic activity may be most required. EXAMPLE 12: Granulocytic cells prepared in accordance with the methods of the invention promote expansion of PBMCs in co-culture The inventors have shown that granulocytic cells (IMANs of the invention) are able to exert therapeutic activity in the treatment of cancer or of infections via their impact on PBMCs (primarily consisting of immune cells such as lymphocytes (including T cells, B cells, and natural killer cells), monocytes, and dendritic cells). In this study, the inventors co-cultured granulocytic cells of the invention (IMANs produced using UM729 without interleukin supplementation according to the method of Example 3)), reference cells, and comparator cells, with PBMCs, with or without G-CSF supplementation. Numbers of the granulocytic cells (IMANs) and PBMCs were assessed over time. The results (shown in Figure 6) demonstrate that all granulocytic cells (IMANs) tested shared the ability to induce an increase in PBMC numbers (particularly after 24 hours of culture). This indicates that the cells of the invention (IMAns) may be expected to exert the same beneficial therapeutic effects when used to treat conditions such as cancer or infection in vivo, following administration to an organism (e.g. mice) or subject (e.g. human subject). It is also notable that the cells of the invention (IMANs) exhibited persistence in in vitro culture that was increased as compared to the comparator cells, and comparable with that seen in respect of the reference cells. EXAMPLE 13: Comparison, after 7 days of in vitro culture, of granulocytic cells prepared in accordance with the methods of the invention and comparator cells Populations of cells of the invention (IMANs) and comparator cells were cultured for seven days in vitro, and subject to flow cytometry assessment. The results of this assessment are set out as a series of plots in Figure 7. As can be seen from this figure, cells of the invention (IMANs produced using UM729 without interleukin supplementation according to the method of Example 3) demonstrated favourable properties as compared to the comparator cells (produced by a method using culture medium v0.3c, Table 9) in each of the metrics assessed. The total number of cells and proportion of live cells was increased as compared to comparator cells. Furthermore, the cells of the invention (IMANs) demonstrated increased markers associated with granulocyte lineage (CD15 and CD66b), and in particular with neutrophil lineage and function (neutrophil elastase and MPO), as compared to the comparator cells. These results demonstrate the advantages of the methods of the invention, both in terms of their ability to yield increased numbers of cells (IMANs) (and greater proportion of viable cells), and to yield cells (IMANs) demonstrating improved biological and therapeutic characteristics (increased neutrophil markers and granule constituents). EXAMPLE 14: Inclusion of a pyrimido-[4,5-b]-indole derivative in methods of the invention increases homogeneity of granulocytic cells produced The methods of the invention utilise a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells. The inventors have found that inclusion of such an agent in the cell culture conditions used offers a number of advantages in practice. In the present study, the inventors investigated the effect of the presence of a pyrimido-[4,5- b]-indole derivative (UM729) on the homogeneity of granulocytic cell populations produced using the methods of the invention (with or without interleukin supplementation). The results are shown in Figure 8. These results suggest that IMDM without UM729 provides the largest proportion of committed myeloid cells. This is a disadvantage as subsequent studies showed an unfavourable lower CD34 expression at the end of expansion (at E8) prior to differentiation, which led to lower persistence. While a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells may be expected to increase cell numbers, Figure 8 demonstrates that presence of such an agent during the expansion phase of the methods of the invention surprisingly has a beneficial impact in improving homogeneity of the cell populations produced. Figure 8 also demonstrates that this effect may be further enhanced by selection of the basal medium used in the cell culture conditions. EXAMPLE 15: Granulocytic cells produced by methods of the invention incorporating the pyrimido-[4,5-b]-indole derivative UM171 demonstrate greater cancer cell killing activity than those produced by methods incorporating the pyrimido-[4,5-b]-indole derivative UM729 Cancer cell killing activity of granulocytic cells (IMANs) produced by methods of the invention utilising the pyrimido-[4,5-b]-indole derivative UM171 (e.g. according to the method of Example 5 or 6) was compared with that of cells produced by methods utilising UM729 (e.g. according to the method of Example 3 (both methods without interleukin supplementation). The granulocytic cells of the invention (IMANs) were incubated with cells of the non-small cell lung cancer line A549 at effector:target (E:T) ratios of 20:1 or 40:1, and percentage lysis of the cancer cells calculated. The results of this study are set out in Figure 9. It was found that on average 24.6% lysis of A549s was achieved at an E:T ratio of 20:1 for cells of donor NTP016 across multiple regimens. This increased to 63.8% lysis of A549s at an E:T ratio of 40:1 for the same donor. These are consistently higher than the A549 lysis values achieved when UM729 was added to the cell culture conditions: 5.4% and 44.4% at an E:T ratio of 20:1 and 40:1 respectively. These results show the improvement in cancer cell killing that has been demonstrated by the addition of UM171 in place of UM729. Importantly, methods of the invention comprising UM729 still were able to show increases in cancer cell killing over previous methods, as shown in Example 7 (Figure 1). SUMMARY OF RESULTS OBTAINED BY THE INVENTORS Results obtained investigating expansion phase conditions: • Methods of the invention without interleukin supplementation of expansion media (process v0.4d) using 1E6 cell seeding at E4 continued to maintain stemness on average to >70% at E8. This was comparatively greater than conditions which included IL-3 and IL-6 in expansion media (process v0.4c). • Overall, v0.4d process on average illustrated > 500-fold expansion capacity. • Extended characterisation, looking at expression within CD34+ and CD34- populations, v0.4d has lower expression of CD71, CD38 and CD45RA than v0.4c exhibiting maintenance of a more stem population. In addition, for CD34- populations, v0.4d also had lower expression of differentiation markers CD11b and CD15 compared to v0.4c. Results obtained investigating expansion phase conditions: • v0.4d process resulted in IMANs which exhibited higher commitment towards the myeloid lineage in a shorter period of time, which has ultimately led to a more homogenous cell product which can be produced on a shorter time scale (E8D4). • v0.4d process results in higher expression of markers associated with neutrophil anti- tumour functionality, e.g. CD89 and FAS-L, whilst also expressing high levels of CD71 which is associated with neutrophil progenitor cells. • v0.4d process produces IMANs which express reduced stem and early progenitor markers at the end of differentiation, namely CD34 and HLA-DR, reducing the safety risks upon drug administration. • v0.4d retains low CXCR4 expression at the end of differentiation, suggesting cells will not home to the bone marrow. Results comparing products of methods using UM171 and UM729: The inventors compared the properties of cells (IMANs) produced in methods of the invention practiced using UM171 and those practiced using UM729. The data (not shown) noted no significant differences in terms of: • Expansion phase phenotype, • Myeloid phenotypic markers • Post-thaw recovery • Total expansion of cell numbers. Results of characterisation of the cells of the invention: • Whilst development continues in respect of post-thaw cell recovery, v0.4d optimal process still showed ~70% recovery when freezing with Cool Cells. • On average 40% cell killing activity was observed across all the donors at 40:1 E:T in a co-culture of cells of the invention (IMANs) directly post thaw with A549 tumour cells. • Initial test of tri-culture of A549, cells of the invention (IMANs) and PBMCs was successful to show a response from multiple mechanisms of action (MoAs) which is greater than IMANs only. • Cells of the invention (IMANs) from all process alterations can activate NK cell fraction during 48 hour co-culture. Upregulation of OX40 and 4-1BB are observed. • Population of cells of the invention were characterised as comprising granulocytes, or precursors (e.g. granulocyte precursor comprising promyelocytes, myelocytes and / or intermediate cells thereof) thereof, wherein: • between 55% and 65% of the cells of the population express CD11b, • between 70% and 90% of the cells of the population express CD15, • between 70% and 90% of the cells of the population express CD64, • between 75% and 95% of the cells of the population express CD89, • between 50% and 70% of the cells of the population express CXCR2, • between 60% and 80% of the cells of the population express neutrophil elastase, • between 0% and 10% of the cells of the population express CD14, • between 0% and 2.5% of the cells of the population express CD19, • between 0% and 2.5% of the cells of the population express CD3, • between 0% and 10% of the cells of the population express CD34, • between 0% and 20% of the cells of the population express CD66b, • between 0% and 2.5% of the cells of the population express CD68, • between 20% and 40% of the cells of the population express CXCR4, and • between 20% and 40% of the cells of the population express HLA-DR. EXAMPLE 16: Characterisation of granulocyte progenitor cells produced by methods of the invention after 8 days of expansion The inventors undertook a study to characterise the granulocyte progenitor cells produced in the methods of the invention. The results are set out in Figure 10, which shows the percentage expression of a range of markers expressed by granulocyte progenitor cells produced by methods of the invention after expansion for three different donors. EXAMPLES 17 TO 23: Impact of granulocytic cells of the invention on adoptive immunotherapy cells The inventors undertook a number of studies to investigate the effects of granulocytic cells of the invention (IMANs) on cells suitable for use in adoptive immunotherapy. In particular, the impact of granulocytic cells of the invention (IMANs) on cells expressing chimeric antigen receptors (CARs), as exemplified by CAR-T cells expressing CAR specific to the tumour associated antigen HER2, was investigated. Examples 17 to 21 utilised CAR T-cells that were autologous to the granulocytic cells of the invention, whereas Examples 22 and 23 used allogeneic CAR-T cells. Example 17 used comparator cells as proof of principle. Examples 18 to 21 used granulocytic cells of the invention (IMANs) produced using a method of the invention incorporating supplementation with interleukins in the expansion phase (v0.4c), while Examples 10 and 11 used granulocytic cells of the invention (IMANs) produced using a method of the invention without supplementation with interleukins in the expansion phase (v0.4d). EXAMPLE 17: Granulocytic cells enhance activation of CAR-T cells in response to stimulatio The inventors assessed the ability of granulocytic cells (IMANs of the invention) to immunomodulate autologous CAR-T cells. CAR-T cells were cultured either on their own, or in co-culture with granulocytic cells (IMANs), at different concentrations of conditions (“Transact”, Miltenyi Biotec) causing TCR stimulation. The CAR-T cells’ expression of activation markers (4-1bb, CD69 and CD25) was then assessed. The results of this study are set out in Figure 11. Here it can be seen that, both CAR-T cultures and CAR-T / granulocytic cell (IMANs) co-cultures exhibited increased expression of each of the activation markers assessed in response to increasing concentration of the activation conditions. However, the expression of each of the activation markers by CAR-T cells was significantly increased by co-culture with granulocytic cells (IMANs) at each concentration tested. These data suggest that use of granulocytic cells (IMANs) in combination with CAR-T cells should offer advantages in terms of increasing the activation of the CAR-T cells. This is likely to be beneficial in a wide range of therapeutic contexts in which CAR-T cells may be employed. EXAMPLE 18: Granulocytic cells of the invention increase CAR-T cell numbers and proportion of T cells expressing CARs, overcoming cancer cell mediated downregulation The inventors assessed the number of CAR-T cells and proportion of CAR+ T cells in cultures incubated with cells of the SK-OV-3 ovarian cancer cell line. CAR-T cells were either cultured on their own with the cancer cells, co-cultured with cancer cells and with granulocytic cells of the invention (IMANs). Assessment of cell numbers and CAR expression was undertaken after 72 hours of culture. The results are set out in Figure 12. The left-hand panel of this figure shows the impact of the presence of cancer cells, and of granulocytic cells of the invention (IMANs), on CAR-T cell numbers. Presence of cells from the ovarian cancer cell line caused a relatively small increase in the number of CAR-T cells present in culture. Addition of granulocytic cells of the invention (IMANs) to the culture markedly increased the number of CAR-T cells present. This indicates that use of granulocytic cells of the invention (IMANs) in therapies with CAR-T cells is likely to increase the number of CAR-T cells present in a subject receiving such treatment (and particularly at sites where cancer cells are present), which can be expected to offer significant benefits in use. The right-hand panel of Figure 12 demonstrates the impact of the presence of cancer cells, and of granulocytic cells of the invention (IMANs), on the proportion of CAR-T cells expressing CARs. Here it can be seen that addition of cancer cells to culture with CAR-T cells induces a reduction in the proportion of these cells that express CARs. This down- regulation of CAR expression upon target engagement is a known problem associated with CAR-T cell therapies. However, it can further be seen that the addition of granulocytic cells of the invention (IMANs) in co-culture with the CAR-T cells causes a near two-fold increase in the proportion of CAR+ cells, restoring the levels of expression to those found in the absence of cancer cells. Thus, the use of granulocytic cells in accordance with the invention (IMANs) in combination with CAR-T cells (or other immune cells expressing CARs) may provide a benefit in terms of reducing cancer-mediated downregulation of CAR expression. This may increase and prolong the efficacy of CAR expressing cells in therapeutic use. EXAMPLE 19: Granulocytic cells of the invention increase CAR-T cell activation in response to cancer cells The inventors investigated expression by CAR-T cells of the activation markers CD25, CD69 and 4-1bb in response to culture with cancer cells of the SK-OV-3 ovarian cancer cell line. Cells were grown in the presence or absence of granulocytic cells of the invention (IMANs), and expression of activation markers was assessed after 72 hours. The results of this study are set out in Figure 13. This Figure shows results obtained on the basis of analysis of CAR-T cell and untransduced control T cell populations, or of flow cytometry gated solely on CAR-T cells. The results illustrate that when CAR-T cells are co-cultured with granulocytic cells of the invention (IMANs), and in the presence of cells of a cancer cell line, they exhibit a marked increase in the expression of the activation markers CD25 and 4-1bb as compared to CAR-T cells cultured with cancer cells alone. In the case of 4-1bb, an almost two-fold increase in expression was observed in the mixed population of both transduced and untransduced T cells. While presence of the granulocytic cells of the invention (IMANs) also increases the expression of these activation markers in untransduced cells (as seen in Figure 13), the extent of activation achieved is much lower than in cells expressing CARs. It will be noted that the same pattern of increased expression, relative to CAR-T cells cultured without granulocytic cells of the invention (IMANs), is not observed in respect of CD69. It is known that CD69 represents a marker of activation than is expressed at an earlier timepoint than either CD25 or 4-1bb. Without wishing to be bound by any hypothesis, the inventors believe that assessment at 72 hours may occur too late to observe an increased response in CAR-T cells cultured with the granulocytic cells of the invention (IMANs). Taken as a whole, the results of this study suggest that combining granulocytic cells of the invention (IMANs) with immune cells expressing CARs, such as the CAR-T cells used in this study, significantly increases the activation of the cells expressing CARs in response to the presence of cancer cells. It is also worth noting that the T cells used in this study were from populations that had been extensively expanded in vitro prior to this use. Accordingly, these results also indicate that the granulocytic cells of the invention (IMANs) may have application in overcoming T cell exhaustion. This property may be advantageous in any combination therapy in which granulocytic cells of the invention (IMANs) are used with T cells, including (but not limited to) combination therapies using granulocytic cells of the invention and CAR-T cells. EXAMPLE 20: Granulocytic cells of the invention increase CAR-T cells numbers and CAR expression, when cultured with cancer cells The impact of the presence of granulocytic cells of the invention (IMANs) on numbers of CAR-T cells present after 72 hours of co-culture with cancer cells (SK-OV-3) was investigated. CAR-T cells were cultured at a 10:1 effector:target cell ratio, with or without the presence of granulocytic cells of the invention (IMANs) (also at a 10:1 ratio with the target cells). The results are shown in Figure 14. Here it can be seen that addition of granulocytic cells of the invention (IMANs) in co-culture with the CAR-T cells and cancer cells caused a significant increase in the number of CAR-T cells present (increased by over 1.5-fold as compared to cultures of only CAR-T and cancer cells). Addition of granulocytic cells of the invention (IMANs) to the co-cultures had an even more pronounced effect on the proportion of CAR-T cells expressing CARs within the cultures. As noted above, it is known that engagement of CARs with their targets can cause downregulation of CAR expression. After 72 hours of co-culture with SK-OV-3 cancer cells (in the absence of granulocytic cells of the invention) it can be seen that only around 1.5% of T cells present remained CAR+. In contrast, when granulocytic cells of the invention (IMANS-s) were added to the cultures, the proportion of T cells expressing CARs rose to almost 4%. These results suggest that granulocytic cells of the invention (IMANs) can play a beneficial role in increasing the number of CAR-T cells available to exert a therapeutic effect, and further strengthen the suggestion that they can act to counter the down-regulation of CAR expression that may otherwise occur after engagement of CAR-T cells with their targets. EXAMPLE 21: Impact of granulocytic cells of the invention on CAR-T cell killing of cancer cells The impact of granulocytic cells of the invention (IMANs) on the capacity of CAR-T cells to kill cancer cells in culture was investigated. CAR-T cells were co-cultured with SK-OV-3 cells at an effector:target cell ratio of 10:1, with or without the presence of granulocytic cells of the invention (IMANs) (also at an effector:target cell ratio of 10:1). The results of this study are shown in Figure 15. Initial results (shown in the left-hand panel of Figure 15), indicated that, over 72 hours in co- culture, the presence of granulocytic cells of the invention (IMANs) had little impact on the CAR-T cells’ ability to kill SK-OV-3 cancer cells. The inventors hypothesised that this was due to “saturated” conditions, in which CAR-T cell cancer killing is maximised to an extent that there is little possibility to increase the activity observed. To test this, a further study was performed in which 200,000 additional SK-OV-3 cells were added to the co-cultures after 72 hours. The results of this are shown in the right-hand panel of Figure 15. Here it can be seen that after further cancer cells had been added, these were cleared faster in the samples where CAR-T cells were co-cultured with granulocytic cells of the invention (IMANs), than in samples containing only the cancer cells and CAR-T cells. The inventors believe (without wishing to be bound by any theories) this to demonstrate the effective anti-cancer activity of the increased number of CAR-T cells that occur when granulocytic cells of the invention (IMANs) are added to CAR-T cultures (in keeping with the results set out in previous examples above). Accordingly, these results add further weight to the suggestion that use of granulocytic cells of the invention (IMANs) with adoptive immunotherapies may increase the effectiveness of such therapies. EXAMPLE 22: Granulocytic cells of the invention exert a dose dependent effect on CAR-T cell survival and activation in co-cultures Populations of CAR-T cells were thawed and cultured with allogeneic granulocytic cells of the invention (IMANs) at different ratios. Co-cultures comprising granulocytic cells:CAR-T cells at ratios of 0.25:1, 0.5:1, 1:1, 2.5:1 or 5:1 were compared with CAR-T cells cultured on their own for the same period of time. Survival of the CAR-T cells, and their expression of a panel of activation markers, was assessed after culture for 96 hours. As can be seen from the results set out in Figure 16, cultures of CAR-T cells alone yielded around 1,500 live T cells. In contrast, the number of live T cells remaining in co-cultures of granulocytic cells of the invention (IMANs) and CAR-T cells increased in a dose dependent manner. When cultured at a ratio of 5 granulocytic cells:1 CAR-T cells, around 21,000 live T cells were observed, an approximately 15-fold increase in T cell numbers. Similar dose dependent increases were noted in respect of the activation markers 4-1bb, CD25, CD69 and OX40. Even the lowest ratios of granulocytic cells:CAR-T cells (0.25:1) resulted in significant increases in expression of these markers, as compared to cultures of cancer cells and CAR-T cells alone. As with cell survival, expression of activation markers was also increased 15-fold or more at higher ratios (5:1 or 10:1). These results provide a clear indication that treatments using granulocytic cells of the invention (IMANs) in combination with cells (such as the CAR-T cells tested) that express CARs, will offer significant advantages in use. The skilled person will understand that the increased survival of CAR-T cells, and their increased expression of activation markers, may be expected to give rise to more effective therapies. EXAMPLE 23: Granulocytic cells of the invention enhance survival and cytotoxicity of adoptive T cell therapies Thaw CAR-T cells. Culture for a period of 72 hours, without cytokine supplementation, either on their own, or in the presence of granulocytic cells of the invention (IMANs). At that point, cells of the SK-OV-3 cancer cell line were added to the cultures. Numbers of CAR-T cells and of cancer cells were then observed over 96 hours, to allow an assessment of CAR-T cell survival and expansion, and of tumour cell lysis. The results are shown in Figure 17. In cultures of CAR-T cells without granulocytic cells of the invention (IMANs), the number of cells present dropped by approximately 95% over the 72 hour period of culture without cytokine supplementation. In contrast, when the CAR-T cells were cultured with granulocytic cells of the invention (IMANs), cell numbers only dropped by around 30% over the same period. The reactions of the cells to the addition of SK-OV-3 cancer cells also differed dramatically. Normally, it would be expected that introduction of cells expressing a TAA recognised by a CAR would lead to a rapid expansion of numbers of the CAR-expressing cells. However, to the inventors’ surprise, no such response was observed in respect of the CAR-T cells that had been cultured for 72 hours in the absence of granulocytic cells of the invention (IMANs). Instead, the CAR-T cell numbers continued to decline, so that none remained after 96 hours of culture. In contrast, when cancer cells were introduced to the CAR-T cells co-cultured with granulocytic cells of the invention (IMANs), the numbers of CAR-T cells increased rapidly over the next 96 hours. In these populations addition of the cancer cells caused the CAR-T numbers to rally. By 96 hours of culture an approximately 2.5-fold increase had been achieved as compared to the number of CAR-T cells introduced at the beginning of the study, and nearly 4-fold as compared to the number of CAR-T cells present when the cancer cells were added. These differences in cell numbers were also reflected in cancer cell killing activity of the CAR-T cells cultured with or without granulocytic cells of the invention (IMANs). CAR-T cells culture with granulocytic cells of the invention (IMANs) achieved almost full clearance of the SK-OV-3 cells introduced within about 72 hours. In contrast, the cultures of CAR-T cells grown without granulocytic cells of the invention (IMANs) did not reduce cancer cell numbers as compared to control populations containing cancer cells alone. In light of the above, the inventors believe (without wishing to be bound by any theories) that the granulocytic cells of the invention (IMANs) may suitably have beneficial uses in combination therapies with adoptive cells of the immune system, such as CAR-T cells. The use of granulocytic cells of the invention (IMANs) in this manner may enhance the survival of the adoptive immune cells (without these cells requiring cytokine supplementation) and may increasing the adoptive immune cells’ therapeutic activity (and in particular their cytotoxic activity). Materials and reagents used in the Examples The materials used in the methods of preparing granulocytes, or granulocyte precursor cells, (also referred to herein as “IMANs” or “IMANps”) described above were as follows:

[0004] Table 1 – Reagents and Equipment used in the methods of the invention described in Examples 1-4 Material Supplier Part No. Cryostor10 cryopreservation medium Sigma C2874-100ML FLT-3L (Research grade) Peprotech 300-19-500uG G-CSF (Research grade) Peprotech 300-23-500uG GM-CSF (Research grade) Biotechne 215-GM-050 HSA Octapharma 5400949 IL-3 (Research grade) Peprotech 200-03-500uG IL-6 (Research grade) Peprotech 200-06-100uG IMDM (Phenol red free) Life Technologies 21056023 ITS Life Technologies 41400045 Penicillin / streptomycin Life Technologies 15140122 SCF (Research grade) Peprotech 300-07-500uG Stemline II Sigma S0192-500ML TNFα (Research grade) Peprotech 300-01A-50uG TPO (Research grade) Peprotech 300-18-500UG UM729 Stemcell 72332 Technologies G-Rex 6M Wilson Wolf 80660M

[0005] Table 2 – Materials used for analytical testing; Examples 1-4 Material Supplier Cat. No. BD Cellfix 10X BD 349202 Human TruStain FcXTM(Fc BioLegend 422302 Receptor Blocking Solution) Efluor780 Live / dead stain Life Technologies (Invitrogen / 65-0865-14 Applied Biosystem) Solution 18, AO-DAPI Staining Chemometec 910-3018 Reagent ONE-Glo™ Luciferase Assay Promega E6130 System, 1L Staurosporine solution from Merck Life Science UK Limited S6942-200UL Streptomyces sp., Ready Made Solution, 1 mM in DMSO Fetal Bovine Serum, qualified, Life Technologies 10500064 heat inactivated. (Invitrogen / Applied Biosystem) DMEM High with Glutamax – I Life Technologies 61965026 (Invitrogen / Applied Biosystem)

[0006] Table 3 - Reagents and Equipment used in the methods of the invention described in Example 5 Material Supplier Cat. No IMDM with high glucose, Life Technologies (Invitrogen / 21056023 (or glutamine, HEPES, sodium Applied Biosystem) equivalent) pyruvate (no phenol red) Stemline II Sigma SO129-500 ML UM171 Biosynth yhc72409-1mg ITS Life Technologies (Invitrogen / 41400045 Applied Biosystem) HSA Octapharma 5400949 G-Rex 6M well plate Wilson Wolf 80660M G-Rex 100M – Open system Wilson Wolf RU81100 CryoStor CS10, cryopreserva- Merck Life Science UK Limited C2874-100 ML tion medium 500 ml PBS, pH 7.4, Gibco Fisher Scientific 15374875 GMP FLT-3L Biotechne BT-FT3L-GMP-01M GMP SCF ThermoFisher Scientific GMP300-07 GMP TPO Biotechne 288E-GMP GMP G-CSF BioLegend 578616 GMP GM-CSF Biotechne 215-GMP-050 GMP IL-3 ThermoFisher Scientific GMP200-03 GMP TNFα Biotechne 210-GMP-100 Reagents used for in process – flow cytometry phenotyping (E0 – E8D4; post-thaw) were as follows: Table 4: In process neutrophil phenotype markers; Examples 1-5 In process neutrophil phenotype v3 Fluorochrome Antigen Clone Isotype Supplier Cat # V1 BV421 CD34 561 Mouse BioLegend 343610 IgG2a V4 BV605 CD11b M1 / 70 Rat IgG2b BioLegend 101257 V5 BV650 CD71 CY1G4 Mouse BioLegend 334116 IgG2a B1 VioBright B515 CD45RA REA REA562 Miltenyi 130-113- 362 B2 PE HLA-DR L243 Mouse BioLegend 307606 IgG2a B5 PerCpCy5.5 CD33 WM53 Mouse BioLegend 303414 IgG1 B6 PE-Cy7 CD49d 9F10 Mouse BioLegend 304314 IgG1 R1 APC CD15 HI98 Mouse IgM BioLegend 301908 R2 AF700 CD38 HIT2 Mouse BioLegend 303524 IgG1 R3 A780 Live / dead Neutrophil Phenotype (E8D0 – E8D4; post-thaw) Table 5: Markers of neutrophil phenotype; used in Examples 1-5 Neutrophil phenotype Fluorochrome Antigen Clone Isotype Supplier Cat # V1 BV421 CD40 5C3 Mouse BioLegend 334332 IgG1 V4 BV605 CD11b M1 / 70 Rat IgG2b BioLegend 101257 V5 BV650 HLA-DR L234 Mouse BioLegend 307650 IgG2a B1 VioBright B515 CXCR4 REA649 REA Miltenyi 130-120- 025 B2 PE CD54 HA58 Mouse BioLegend 353106 IgG1 B5 PerCpCy5.5 CXCR2 5E8 / CXCR2 Mouse BioLegend 320718 IgG1 B6 PE-Cy7 CD89 A59 Mouse BioLegend 354108 IgG1 R1 APC CD15 HI98 Mouse IgM BioLegend 301908 R2 AF700 CD11c Bu15 Mouse BioLegend 337220 IgG1 R3 A780 Live / dead

[0007] Table 6: markers of neutrophil activation; used in Examples 1-5 Neutrophil activation Fluorochrome Antigen Clone Isotype Supplier Cat # V1 BV421 CD177 MEM- Mouse BD 564240 166 IgG1 V4 BV605 CD11b M1 / 70 Rat IgG2b BioLegend 101257 V5 BV650 HLA-DR L234 Mouse BioLegend 307650 IgG2a B1 VioBright B515 CD66b REA306 REA Miltenyi 130-126- 905 B2 PE CD16 3G8 Mouse BioLegend 302008 IgG1 B5 PerCpCy5.5 CD10 HI10a Mouse BioLegend 3122156 IgG1 B6 PE-Cy7 CD18 TS1 / 18 Mouse BioLegend 302118 IgG1 R1 APC CD15 HI98 Mouse IgM BioLegend 301908 R2 AF700 FAS-L 100419 Mouse Biotechne FAB126N- IgG2 100UG R3 A780 Live / dead

[0008] Neutrophil granules Table 7: Markers of neutrophil granules; used in Examples 1-5 Neutrophil granules Fluorochrome Antigen Clone Isotype Supplier Cat # V1 BV421 V4 BV605 CD11b M1 / 70 Rat IgG2b BioLegend 101257 V5 BV650 HLA-DR L234 Mouse BioLegend 307650 IgG2a B1 VioBright B515 MPO REA491 REA Miltenyi 130-129- 211 B2 PE Neutrophil NP57 Mouse BD 568909 elastase IgG1 B5 PerCpCy5.5 Cathepsin Rabbit IgG Stratech BS- G 1598R- PERCP- CY5.5- BSS B6 PE-Cy7 Granzyme GM26E7 Mouse BioLegend 370516 K IgG1 R1 APC CD15 HI98 Mouse BioLegend 301908 IgM R2 AF700 R3 A780 Live / dead Off target Table 8: Markers of off target differentiation; used in Examples 1-5 Off target Fluorochrome Antigen Clone Isotype Supplier Cat # V1 BV421 CD14 HCD14 Mouse BioLegend 325606 IgG1 V4 BV605 CD11b M1 / 70 Rat IgG2b BioLegend 101257 V5 BV650 HLA-DR L234 Mouse BioLegend 307650 IgG2a B1 VioBright B515 CD16 REA423 REA Miltenyi 130-119- 616 B2 PE CD19 Mouse BioLegend IgG1 B5 PerCpCy5.5 CD86 IT2.2 Mouse BioLegend 305420 IgG2b B6 PE-Cy7 CD68 Y1 / 82A Mouse BioLegend 333816 IgG2b R1 APC CD15 HI98 Mouse BioLegend 301908 IgM R2 AF700 CD11c Bu15 Mouse BioLegend 337220 IgG1 R3 A780 Live / dead Table 9: Description of the culture medium components (and specific amounts thereof) used in methods v0.4c, and v0.4d for generating the granulocyte precursor cells of the invention (IMANs) as well as culture medium components (and specific amounts thereof) used in method v0.3c for generating comparative cells. Phases Components (amounts) per method version v0.3c v0.4c v0.4d IMDM IMDM IMDM 1% (W / V) HSA 1% (W / V) HSA 1% (W / V) HSA 1x ITS 1x ITS 1x ITS Expansion SCF 200 ng / mL SCF 20...

Claims

CLAIMS 1. A granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell comprises: a. increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or b. decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo.

2. The granulocyte precursor cell according to claim 1, wherein the granulocyte precursor cell has been differentiated in vitro from a stem cell derived from a donor having granulocytes (preferably neutrophils) with high cancer killing activity (CKA).

3. The granulocyte precursor cell according to claim 2, wherein the CKA is assessed by a method comprising: a. admixing granulocytes (preferably neutrophils) from a donor with cancer cells; b. incubating said admixture; and c. measuring the % of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (preferably neutrophils).

4. The granulocyte precursor cell according to claim 3, wherein the granulocytes (preferably neutrophils) have a CKA of at least 30%, preferably at least 50%, more preferably at least 70%.

5. The granulocyte precursor cell according to any one of the preceding claims, wherein the equivalent granulocyte precursor cell that has been differentiated in vivo is a peripheral blood-derived granulocyte precursor cell, preferably wherein the granulocyte precursor cell is a promyelocyte, a myelocyte, or an intermediate thereof.

6. The granulocyte precursor cell according to any one of the preceding claims, wherein the increased expression and / or decreased expression is not the result of a genetic modification of the granulocyte precursor cell differentiated in vitro.

7. The granulocyte precursor cells according to any one of claim 2-6, wherein the stem cell is an haematopoietic stem cell (HSC).

8. The granulocyte precursor cell according to any one of the preceding claims, wherein the granulocyte precursor cell that has been differentiated in vitro is a promyelocyte, a myelocyte, or an intermediate thereof.

9. A method of preparing cells (e.g. granulocyte precursor cells) for therapeutic use, the method comprising culturing a population of stem cells (preferably HSCs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte progenitor cells comprise the presence of (i) SCF; (ii) FLT-3 ligand; (iii) TPO; and (iv) a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSC.

10. The method according to claim 9, wherein the population of stem cells has been derived from a donor having granulocytes (preferably neutrophils) with high CKA.

11. The method according to claim 10, wherein the CKA is assessed by a method comprising: a. admixing granulocytes (preferably neutrophils) from a donor with cancer cells; b. incubating said admixture; and c. measuring the % of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (preferably neutrophils).

12. The method according to claim 11, wherein the granulocytes (preferably neutrophils) have a CKA of at least 30%, preferably at least 50%, more preferably at least 70%.

13. The method according to any one of claims 9-12, wherein the pyrimido-[4,5-b]-indole derivative is provided at a concentration within the range of 15nM - 1.5µM.

14. The method according to any one of claims 9-13, wherein the pyrimido-[4,5-b]-indole derivative is one of: UM171 or UM729, preferably UM171.

15. The method according to any one of claims 9-14, wherein the cell culture conditions further comprise: ITS; and / or HSA.

16. The method according to claim 15, wherein the cell culture conditions comprise one or more conditions independently selected from the group consisting of: a. SCF at a concentration of approximately 0.1-0.2 µg / ml; b. FLT-3 ligand at a concentration of approximately 0.1-0.2 µg / ml; c. TPO at a concentration of approximately 0.01-0.02 µg / ml; and d. HSA at a concentration of approximately 1%.

17. The method of claim 16, wherein the cell culture conditions comprise (e.g. further comprise): IL-3 at a concentration of approximately 0.0001-0.015 µg / ml; and / or IL-6 at a concentration of approximately 0.0001-0.015 µg / ml.

18. A method of preparing cells (e.g. granulocytes or granulocyte precursors, preferably granulocyte precursor cells) for therapeutic use, the method comprising culturing a population of granulocyte progenitor cells in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or granulocyte precursors (preferably granulocyte precursor cells), the cell culture conditions comprising the presence of: (i) a basal medium; (ii) SCF; (iii) TPO; and(iv) G-CSF.

19. The method according to claim 18, wherein the population of granulocyte progenitor cells have been produced by a method according to any one of claims 9-17.

20. The method according to claim 18 or claim 19, wherein each of SCF, TPO, and G- CSF are provided in first and second incidences of administration during the culturing in conditions that promote differentiation into granulocytes, or precursors thereof (preferably granulocyte precursor cells).

21. The method according to claim 20, wherein the amount of each of SCF, TPO, and G- CSF provided in the second incidence of administration is approximately double that provided in the first incidence of administration (preferably is double that provided in the first incidence of administration).

22. The method according to claim 20 or claim 21 wherein the amount of each of SCF, TPO, and G-CSF provided in the first incidence of administration is approximately 0.333 ng per 1000 cells (preferably is 0.333 ng per 1000 cells).

23. The method according to anyone of claims 20-22, wherein the concentration of each of SCF, TPO, and G-CSF provided in the second incidence of administration is approximately 0.666 ng per 1000 cells (preferably is 0.666 ng per 1000 cells).

24. The method according to any one of claims 18-23, wherein the cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells), further comprise: GM-CSF at a concentration of approximately 0.01 µg / ml; and IL-3 at a concentration of approximately 0.13 µg / ml; and TNFa at a concentration of approximately 0.001µg / ml.

25. The method according to claim 24, wherein GM-CSF and IL-3 are provided to the cells (preferably granulocyte precursor cells) for the final 48 hours of a period ofculture in conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells).

26. The method according to claim 24, wherein TNFa is provided to the cells (preferably granulocyte precursor cells) for the final 24 hours of a period of culture in conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells).

27. A method of preparing cells (e.g. granulocytes, or precursors thereof, preferably granulocyte precursor cells) for therapeutic use, the method comprising: culturing a population of stem cells (preferably HCSs) in cell culture conditions to produce a population of granulocyte progenitor cells, wherein the cell culture conditions for producing the granulocyte precursor cells comprise the presence of: SCF; FLT-3 ligand; TPO; and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of HSCs; to produce the population of granulocyte progenitor cells, and further comprising culturing the granulocyte progenitor cells of said population in cell culture conditions that promote differentiation of the granulocyte progenitor cells into granulocytes, or precursors thereof (preferably granulocyte precursor cells), the cell culture conditions comprising the presence of: a basal medium; SCF; TPO; and G-CSF.

28. The method according to claim 27, further comprising recovering the granulocytes, or precursors thereof (preferably granulocyte precursor cells).

29. The method according to claim 28, further comprising cryopreserving the granulocytes, or precursors thereof (preferably granulocyte precursor cells).

30. The method according to any one of claims 9-29, wherein the stem cell is an HSC.

31. The method according to any one of claims 9-30, wherein the granulocyte precursor cell is a promyelocyte, a myelocyte, or an intermediate thereof.

32. A granulocyte or granulocyte precursor (preferably granulocyte precursor cell) obtainable by a method according to any of claims 9-31.

33. A granulocyte, or granulocyte precursor (preferably granulocyte precursor cell).

34. The granulocyte, or precursor thereof according to claim 32 or 33, wherein the granulocyte or granulocyte precursor is a granulocyte precursor cell comprising: a. increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or b. decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo.

35. A population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) obtainable by a method according to any of claims 9-31, wherein: (i) between 55% and 65% of the cells of the population express CD11b, (ii) between 70% and 90% of the cells of the population express CD15, (iii) between 70% and 90% of the cells of the population express CD64, (iv) between 75% and 95% of the cells of the population express CD89, (v) between 50% and 70% of the cells of the population express CXCR2, (vi) between 60% and 80% of the cells of the population express neutrophil elastase, (vii) between 0% and 10% of the cells of the population express CD14, (viii) between 0% and 2.5% of the cells of the population express CD19, (ix) between 0% and 2.5% of the cells of the population express CD3,(x) between 0% and 10% of the cells of the population express CD34, (xi) between 0% and 20% of the cells of the population express CD66b, (xii) between 0% and 2.5% of the cells of the population express CD68, (xiii) between 20% and 40% of the cells of the population express CXCR4, and / or (preferably and) (xiv) between 20% and 40% of the cells of the population express HLA-DR.

36. A population of granulocytes, or precursors thereof (preferably granulocyte precursor cells), comprising granulocytes, or precursors thereof (preferably granulocyte precursor cells), wherein: (i) at least 50% of the cells of the population express CD64; and / or (preferably and) (ii) at least 50% of the cells of the population express CD89; and / or neutrophil elastase.

37. A population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells), comprising granulocytes, or granulocyte precursors (preferably granulocyte precursor cells), wherein: (i) at least 50% of the cells of the population express CD64; (ii) at least 50% of the cells of the population express CD89; and / or (preferably and) (iii) at least 50% of the cells of the population express neutrophil elastase.

38. A pharmaceutical composition comprising the granulocyte precursor cells according to any one of claims 1-8, the granulocyte or granulocyte precursor cells (preferably granulocyte precursor cells) according to any one of claims 32-34 or a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any of claims 35-37.

39. The pharmaceutical composition according to claim 38, further comprising G-CSF.

40. A granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one ofclaims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39, for use as a medicament.

41. Use of a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39 in the manufacture of a medicament.

42. A method for treating a disorder comprising administering to a subject in need thereof a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39.

43. A granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39, for use in treating cancer.

44. Use of a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39 in the manufacture of a medicament for treating cancer.

45. A method for treating cancer comprising administering to a subject in need thereof a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one ofclaims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39.

46. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-45, wherein the cancer is one or more of: head and neck cancer, cervical cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach cancer, cervical cancer, ovarian cancer, lung cancer, bladder cancer, kidney cancer, brain cancer, prostate cancer, myeloma cancer, non-Hodgkin’s lymphoma (NHL), larynx cancer, uterine cancer, or breast cancer.

47. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-46, wherein the cancer is head and neck cancer.

48. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-46, wherein the cancer is cervical cancer.

49. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-48 in combination with a CAR-T cell.

50. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-49 in combination with an antibody selected from: Cetuximab, Rituximab, Daratumumab, Tafasitamab, Obinutuzumab, Ofatumumab, Alemtuzumab,Blinatumomab, Lynozyfic, Panitumumab, Bevacizumab, Ramucirumab, Denosumab, Dinutuximab, and Elotuzumab, preferably Cetuximab.

51. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 43-50 in combination with an immune check point inhibitor selected from: Nivolumab, Ipilimumab, Pembrolizumab, Cemiplimab, Durvalumab, Atezolizumab, Relatlimab, Dostarlimab, Avelumab, Tislelizumab, Toripalimab, Sugemalimab, Camrelizumab, and Tremelimumab, preferably Nivolumab.

52. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use, the use, or the method according to any one of claims 49-51, wherein the cancer is selected from head and neck cancer, cervical cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach cancer, cervical cancer, ovarian cancer, lung cancer, bladder cancer, kidney cancer, brain cancer, prostate cancer, myeloma cancer, non-Hodgkin’s lymphoma (NHL), larynx cancer, uterine cancer, and breast cancer, preferably head and neck cancer and / or cervical cancer.

53. A granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39, for use in treating an infection.

54. Use of a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39 in the manufacture of a medicament for treating an infection.

55. A method for treating an infection comprising administering to a subject in need thereof a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39.

56. A granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39, for use in treating an autoimmune disease.

57. Use of a granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37, or a pharmaceutical composition according to claim 38 or 39 in the manufacture of a medicament for treating an autoimmune disease.

58. A method for treating an autoimmune disease comprising administering to a subject in need thereof granulocyte precursor cell according to any one of claims 1-8, a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34, a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35- 37, or a pharmaceutical composition according to claim 38 or 39.

59. A kit comprising: a. a granulocyte precursor cell according to any one of claims 1-8; b. a granulocyte or granulocyte precursor (preferably granulocyte precursor cell) according to any one of claims 32-34; and / orc. a population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) according to any one of claims 35-37; and d. optionally instructions for use of the same in medicine, e.g. in treating cancer and / or an infection and / or an autoimmune disorder.

60. The granulocyte precursor cell, granulocyte or granulocyte precursor (preferably granulocyte precursor cell), population of granulocytes, or granulocyte precursors (preferably granulocyte precursor cells) for use according to claim 49, by: • increasing therapeutic activity of the adoptive immunotherapy cell; or • increasing activation of the adoptive immunotherapy cell; or • reducing CAR-down regulation on target engagement by the adoptive immunotherapy cell; or • increasing accumulation of adoptive immunotherapy cells; or • increasing proliferation of the adoptive immunotherapy cells; or • increasing persistence of the adoptive immunotherapy cells; or • increasing survival of the adoptive immunotherapy cells; or • increasing cytotoxic activity of the adoptive immunotherapy cells; or • decreasing T cell exhaustion of immunotherapy cells.

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