Granulocytes and granulocyte precursors

Abstract

Provided are granulocyte precursor cells, and populations of granulocyte precursor cells, that express chimeric antigen receptors (CARs). The invention further provides pharmaceutical compositions comprising such cells and cell populations, and to the medical uses and methods of treatment employing such pharmaceutical compositions and cell populations. Medical uses may include the treatment of cancer, treatment of infections, and treatment of autoimmune diseases. The invention further provides methods of preparing cells for therapeutic use.

Description

[0001] GRANULOCYTES AND GRANULOCYTE PRECURSORS FIELD OF THE INVENTION The present invention relates to populations of cells, particularly population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) or populations of neutrophils, or precursors thereof, that express chimeric antigen receptors (CARs). In particular, the invention relates to granulocyte precursors expressing CARs, and to populations of granulocyte precursors that contain granulocyte precursor cells expressing CARs. The invention further relates to pharmaceutical compositions comprising populations of such cells, and to the medical uses and methods of treatment employing such pharmaceutical compositions and cell populations. The invention also relates to methods of preparing cells for therapeutic use. 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. 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 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 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 granulocyte precursor cell comprising a chimeric antigen receptor (CAR). This aspect of the invention further provides a population of granulocyte precursor cells, the population comprising granulocyte precursor cells expressing a CAR. In a second aspect, the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a CAR 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 • less than 50% of the cells of the population express HLA-DR. In a third aspect, the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) wherein: • at least 50% of the cells of the population express CD64; and • at least 50% of the cells of the population express CD89; and / or neutrophil elastase. In a fourth aspect, the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) wherein: • at least 50% of the cells of the population express CD64; • at least 50% of the cells of the population express CD89; and • at least 50% of the cells of the population express neutrophil elastase. In a fifth aspect, the invention provides a population of neutrophils, or precursors thereof, comprising neutrophils, or precursors thereof, expressing neutrophil elastase and a chimeric antigen receptor (CAR), and wherein at least 50% of the cells of the population express CD64; and / or CD89. As discussed in more detail elsewhere in the specification, a granulocyte precursor cell of the first aspect of the invention, or a granulocyte precursor cell present in a population of cells of the first, second, third, fourth or fifth aspects of the invention, 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; and / or • 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. Suitably, this gene expression profile may be exhibited by granulocyte precursor cells produced by the thirteenth aspect of the invention, set out below. In a sixth aspect, the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) wherein: • a first subpopulation of cells are CD15+ CD64+ CD18+ CD49d+ CD71+; • a second subpopulation of cells are CD15- CD11b+ / - CD18+ CD49d+ CD32+ HLA- DR-; and • a third subpopulation of cells are CD15- CD11b- HLA-DR+ CD18+ CD49d+ and CD71+. 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 second to sixth aspects of the invention, or encompassing constituent cells of such populations, or cells in accordance with the first aspect of the invention. Populations of cells of the invention of any of the first to fifth aspects of the invention, or constituent cells of such populations, may be produced using the methods of the thirteenth aspect of the invention (referred to as the v0.4 protocol). Populations of cells of the invention of the sixth aspect of the invention, or constituent cells of such populations, may be produced using the methods of the fourteenth aspect of the invention (referred to as the v0.3 protocol). In a seventh 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 first to fifth aspects of the invention. In an eighth aspect, the invention provides a population of cells according to any of the first to fifth aspects of the invention, or a pharmaceutical composition according to the seventh aspect of the invention, for use as a medicament. In a ninth aspect, the invention provides a method of treating a disease or condition comprising providing a therapeutically effective amount of cells of the invention, or 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 cells or population of cells may be in accordance with any of the first to sixth aspects of the invention. Suitably, the pharmaceutical composition of the invention may comprise cells of the first aspect of the invention, or a population of cells in accordance with any of the second to sixth aspects of the invention. In a tenth 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 cells or population of cells may be in accordance with any of the first to sixth aspects of the invention. Suitably, the pharmaceutical composition of the invention may comprise cells of the first aspect of the invention, or a population of cells in accordance with any of the second to sixth aspects of the invention. In a eleventh aspect, the invention provides a method of preparing cells for therapeutic use, the method comprising culturing stem or progenitor cells in cell culture conditions that induce the formation of a granulocyte precursor cell, or a population thereof, in accordance with any of the first to sixth aspects of the invention, wherein the method comprises modifying the cells to express a CAR. It will be appreciated that, given the capacity of the cells to give rise to granulocytes and granulocyte precursor cells, such progenitor cells disclosed in the context of the present invention may be referred to as “granulocyte progenitor cells”. Such cells are defined further elsewhere in the specification. In a twelfth aspect, the invention provides a method of preparing cells for therapeutic use, the method comprising culturing stem or progenitor cells in cell culture conditions that induce the formation of a population of neutrophils, or precursors thereof, in accordance with the sixth aspect of the invention, wherein the method comprises modifying the cells to express a CAR. In a thirteenth aspect, the invention provides a method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells; and modifying the cells to express a CAR. This is the v0.4 protocol referred to above. Suitably these methods of the eleventh, twelfth and thirteenth aspects of the invention may produce cells, or populations of cells, in accordance with the first to fifth aspects of the invention. In a fourteenth aspect, the invention provides a method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, Flt-3 ligand, IL-3, IL-6, and TPO; and modifying the cells to express a CAR. This is the v0.3 protocol referred to above. Suitably the methods of the fourteenth aspect of the invention may produce populations of cells in accordance with the sixth aspect of the invention. The methods in accordance with the eleventh, twelfth, thirteenth and fourteenth aspects of the invention comprise a step of modifying cultured cells so that they express a CAR. As discussed below, the cells may be modified at different points in culture, so that the nature of the cells (e.g. stem cells, progenitor cells, granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) or neutrophils, or precursors thereof) undergoing modification may be adapted accordingly. The modification step may comprise any suitable technique suitable by which the desired cells may be modified such that they express a CAR. As discussed further below, the inventors have found that methods may readily be practiced by transduction of the cells with a nucleic acid that encodes a desired CAR. DETAILED DESCRIPTION OF THE INVENTION The invention is based, at least in part, on the inventors’ finding that populations of therapeutically effective granulocytes (or precursors thereof) or neutrophils (or precursors thereof) exhibit unexpectedly beneficial properties when modified to express CARs. The inventors have developed protocols for the generation of population of granulocytic cells (which they term “IMANs” immunomodulatory alpha neutrophils) that are well suited to use in cell therapies in a range of conditions. They are able to exert direct cytocidal activity against target cells (such as cancer cells), and to provide therapeutic effects by virtue of such activity. Moreover, they are also able to exert an immunomodulatory effect on other immune cells (such as non-granulocytic immune cells) that increases the effectiveness of such cells in the treatment of conditions such as cancer, infections, or autoimmune diseases. The inventors have found that modification of granulocyte precursor cells (for example precursors of IMANs) to express CARs dramatically increases the cytocidal activity of such cells compared to controls that lack CARs. This increase in activity, which includes 15-fold enhancement of cell killing in certain embodiments generated by the inventors, could not have been anticipated based on what was known from the prior art. Furthermore, the inventors have also found that modification to express CARs unexpectedly decreases the degree of variation in activity that may otherwise be observed between populations of cells derived from different sources. By reducing variability between donors or batches of cells, this provides a product with more consistent and reproducible therapeutic properties. It will readily be appreciated that a reduction in variability of this sort will be very desirable in products intended for medical use. While CARs have been used to direct immune cells, such as neutrophils, to targets with which they would not otherwise normally engage, and even to achieve small increases in cytocidal activity of such granulocytic cells, there is nothing in the prior art to suggest the scale or nature of the improvements identified by the inventors when CARs are expressed in the populations of cells of the invention. The invention will now be further described below. DEFINITIONS Cells suitable for use as cells of the invention In the context of the present invention, a granulocyte (or a precursor thereof, such as a granulocyte precursor cell), is preferably a granulocyte (or a precursor thereof, such as a granulocyte precursor cell) that has been differentiated (e.g. by the methods described herein) in vitro. In keeping with this, a “method of the invention” (except for a method of treatment described herein) is preferably an in vitro method. 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 of the invention (for example, the methods of the thirteenth and fourteenth aspects 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. A granulocyte precursor as set out above, which may be a granulocyte precursor cell of the first aspect of the invention, or a granulocyte precursor cell present in a population of cells of the first, second, third, fourth or fifth aspects of the invention, may be characterised with respect to: • 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 • 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. Suitably, a granulocyte precursor cell of the invention may exhibit increased expression of at least two of SRGN, MPO, HLA-DR, CD74, or ELANE when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo.. Suitably, a granulocyte precursor cell of the invention may exhibit increased expression of at least three of SRGN, MPO, HLA-DR, CD74, or ELANE when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. Suitably, a granulocyte precursor cell of the invention may exhibit increased expression of at least four of SRGN, MPO, HLA-DR, CD74, or ELANE. Suitably, a granulocyte precursor cell of the invention may exhibit increased expression of all five of SRGN, MPO, HLA-DR, CD74, or ELANE when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. Alternatively, or additionally, a granulocyte precursor cell of the invention may exhibit decreased expression of at least two of DEFA1, DEFA3, CAMP, BPI, or AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. For example, such a granulocyte precursor cell of the invention may exhibit decreased expression of at least two of DEFA1, DEFA3, CAMP, BPI, or AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo., at least three of DEFA1, DEFA3, CAMP, BPI, or AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo., at least four of DEFA1, DEFA3, CAMP, BPI, or AZU1, or all five of DEFA1, DEFA3, CAMP, BPI, or AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo.. Suitably, a granulocyte precursor cell of the invention exhibits increased expression of all five of SRGN, MPO, HLA-DR, CD74, and ELANE, and decreased expression of all five of DEFA1, DEFA3, CAMP, BPI, and AZU1 when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. 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). 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 (preferably human) granulocytes (preferably neutrophils) obtained from a donor may be determined or measured by any suitable method (in vitro). Suitably, 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 percentage of cancer cells killed in said admixture, thereby assessing the CKA of said granulocytes (neutrophils). Measuring the percentage 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%. Chimeric antigen receptors (CARs) suitable for use in the cells or methods of the invention CARs are chimeric proteins that combine an extracellular antigen-binding domain and intracellular domain. These are typically separated by a transmembrane domain and hinge (or spacer) region. The antigen-binding domain (which is typically an scFv, or similar fragment derived from an antibody) confers the desired specificity on the CAR, and so on the cell expressing the CAR. Once the antigen-binding domain has bound to its cognate antigen, the intracellular cell domain generated signals causing activation of the cell. The intracellular domain typically comprises regions associated with such signalling. The intracellular domain may comprise a signalling domain and a co-stimulatory domain. Various generations of CARs are known to those skilled in the art. Unless the context requires otherwise, a CAR suitable for use in the cells or methods of the invention may belong to any generation. In a suitable embodiment, a CAR suitable for use in cells or methods of the invention is specific for an antigen selected from the group consisting of: a tumour associated antigen (TAA); a pathogen associated antigen; and an autoimmune disease associated antigen. A wide range of TAAs (for purposes of the present invention also considered to encompass tumour specific antigens to TSAs) are known to those skilled in the art, along with the association of these antigens with particular tumours, or groups of tumours, of interest. It will be a routine matter to identify a TAA of interest, and from that to identify an antigen-binding domain specific for the desired domain. In a suitable embodiment the TAA is 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 In a suitable embodiment the CAR is specific for a TAA associated with solid tumours. In a suitable embodiment, the CAR comprises a signalling domain selected from the group consisting of: an OX40 signalling domain; a tumour necrosis factor receptor 1 (TNFR1) signalling domain, such as a TNFR1 mutant signalling domain; a CD3 signalling domain, such as a CD3ζ or CD3ε signalling domain; a CD64 signalling domain; a CD32 signalling domain; a CD16 signalling domain; an FCε R1 signalling domain; and a CD89 signalling domain. Modification of cells to express a CAR The methods of the eleventh to fourteenth aspects of the invention involve modification of cells to express a CAR. In suitable embodiments of such methods, the modification comprises transduction with a nucleic acid encoding the CAR. Suitably, the transduction is carried out by means of a viral vector. By way of example, transduction may be carried out by means of a viral vector selected from the group consisting of: cytomegalovirus (CMV) vectors; lentiviral (LV) vectors; Moloney murine leukaemia virus (MMLV) vectors; and murine stem cell virus (MSCV) vectors. Such vectors have been demonstrated to be effective in practicing the methods of the invention. In a suitable embodiment, a CMV vector is used to transduce cells with a nucleic acid encoding a CAR to modify cells to express a CAR. In a suitable embodiment, a lentiviral vector is used to transduce cells with a nucleic acid encoding a CAR to modify cells to express a CAR. The inventors have found that transduction of the cells using a lentiviral vector provides notable advantages in the modification of granulocytes, or precursors thereof (e.g., granulocyte precursor cells) to express CARs. As set out in more detail below, and in the Examples, the inventors have devised particularly advantageous protocols for the generation of cells of the invention. The inventors’ protocols improve the proportion of cells expressing CARs. Alternatively, or additionally, the inventors’ protocols improve the intensity of CAR expression. Suitably, the protocols devised by the inventors enable higher proportions of CAR-expressing cells, and / or higher intensity of CAR expression by cells, at lower multiplicity of infection (MOI) as compared to reference methods. The timing of the modification of cells to express a CAR may be determined with reference to other features of a method of the invention. In particular, the timing of modification may be determined with reference to expansion or differentiation steps in a method of the invention. Accordingly, in a suitable embodiment the modification of the cells to express a CAR is applied prior to the differentiation step. In a suitable embodiment the modification of the cells to express a CAR is applied during the differentiation step. Modification of the cells to express a CAR may be applied prior to the expansion step. Suitably, modification of the cells to express a CAR may be applied during the expansion step. Alternatively, modification of the cells to express a CAR may be applied after the expansion step. In a suitable embodiment of a method of the invention, modification of the cells to express a CAR is applied between the differentiation step and the expansion step. The inventors have found that in methods of the invention comprising an expansion step, modification of the cells to express a CAR on the first day of expansion is able to give rise to cells of the invention with elevated cytocidal capacity. Thus, in a suitable embodiment of a method of the invention, cells are transduced on the first day of an expansion step. Transduction of the cells with a nucleic acid may comprise incubation of the cells and nucleic acid for a suitable period of time to allow a desired extent of transduction to occur. Suitably incubation may be in the presence of an agent that promotes transduction. Examples of such agents include those selected from the group consisting of: • fibronectin, including the commercial product Retronectin, • Lentiboost® (in particular at a concentration between 0.1mg / ml and 5,000 mg / ml; • poloxamer F108, in particular at a concentration between 01lmg / ml and 5,000 mg / ml; Silibinin, in particular at a concentration between 0.05 μM and 500 μM; Midostaurin, in particular at a concentration between 2nM and 500,000 nM; PEG-PLA-PEG, in particular at a concentration between 1 μg / ml and 5,000 μg / ml; • PEG-PLGA-PEG, in particular at a concentration between 1 μg / ml and 5,000 μg / ml; • PEG-PCL-PEG, in particular at a concentration between 1 μg / ml and 5,000 μg / ml; • Nystatin, in particular at a concentration between 0.1 and 1000 μM; • Natamycin, in particular at a concentration between 0.05 and 500 μM; • Ruxolitinib, in particular at a concentration between 0.01 and 10,000 μM; • Fludarabine, in particular at a concentration between 0.01 and 10,000 μM; • Everolimus, in particular at a concentration between 0.1 and 10 μM; • Resveratrol, in particular at a concentration between 0.1 and 25 μM; • Prostaglandin E, in particular at a concentration between 1 and 100 μM; • Desoxyribonucleosides, in particular at a concentration between 0.1mM and 10mM of each nucleoside; • DMSO, in particular at a concentration between 0.1 and 10% (v / v); and / or • any combination thereof; in particular wherein the one or more additional transduction enhancing compound is selected from the group consisting of: • Lentiboost®, poloxamer F108 and / or a PEG-PCL-PEG polymer. In a suitable embodiment, at least 5% of a population of cells of the invention express a CAR, at least 10% of a population of cells of the invention express a CAR, at least 15% of a population of cells of the invention express a CAR, at least 20% of a population of cells of the invention express a CAR, at least 25% of a population of cells of the invention express a CAR, at least 30% of a population of cells of the invention express a CAR, at least 35% of a population of cells of the invention express a CAR, at least 40% of a population of cells of the invention express a CAR, at least 45% of a population of cells of the invention express a CAR, at least 50% of a population of cells of the invention express a CAR, at least 55% of a population of cells of the invention express a CAR, at least 60% of a population of cells of the invention express a CAR, at least 65% of a population of cells of the invention express a CAR, at least 70% of a population of cells of the invention express a CAR, at least 75% of a population of cells of the invention express a CAR, at least 80% of a population of cells of the invention express a CAR, at least 85% of a population of cells of the invention express a CAR, at least 90% of a population of cells of the invention express a CAR, at least 95% of a population of cells of the invention, or even 100% of a population of cells of the invention express a CAR. Lentiboost® is the proprietary name for a commercially available combination of Poloxamer F108 and polybrene. The inventors have identified that when modifying cells to express a CAR the use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in viral transduction of cells is particularly advantageous. As set out in the Examples, use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the proportion of cells expressing a CAR as compared to other transduction protocols. Use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the proportion of cells expressing a CAR using lower MOIs of a transducing viral vector as compared to other transduction protocols. Use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the intensity of expression of a CAR by modified cells, as compared to other transduction protocols. Use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the intensity of expression of a CAR by modified cells, using lower MOIs of a transducing viral vector as compared to other transduction protocols. Use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the proportion of cells expressing a CAR and to increase the intensity of expression of a CAR by modified cells, as compared to other transduction protocols. Use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR is able to increase the proportion of cells expressing a CAR and to increase the intensity of expression of a CAR by modified cells, using lower MOIs of a transducing viral vector as compared to other transduction protocols. In a suitable embodiment of a method of the invention, transduction performed in the presence of combination of Poloxamer F108 and polybrene (such as Lentiboost®) results in at least 50% of the cells produced by the method expressing a CAR. Such a use of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) in methods of the invention to modify cells to express a CAR may result in 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 even100% of the cells expressing a CAR. In a suitable embodiment of a method of the invention, transduction performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) results in at least 50% of the cells produced by the method expressing a CAR when a viral vector is used at an MOI of 30-100. In a suitable embodiment of a method of the invention, transduction performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) results in at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, of the cells produced expressing a CAR when a viral vector is used at an MOI of 30-100. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) using a viral vector at an MOI of at least 10, at least 20, at least 30, at least 40, at least 50, at least 60, at least 70, at least 80, at least 90, at least 100, at least 150, at least 200, at least 250, at least 300, at least 350, at least 400, at least 450, at least 500, at least 600, at least 700, at least 800, at least 900, or at least 1000 in a method of the invention to modify at least 60% of treated cells to successfully express a CAR. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a a combination of Poloxamer F108 and polybrene (such as Lentiboost®) with a viral vector at an MOI of no more than 10, no more than 20, no more than 30, no more than 40, no more than 50, no more than 60, no more than 70, no more than 80, no more than 90, no more than 100, no more than 150, no more than 200, no more than 250, no more than 300, no more than 350, no more than 400, no more than 450, no more than 500, no more than 600, no more than 700, no more than 800, no more than 900, or no more than 1000 in a method of the invention to modify at least 60% of treated cells to successfully express a CAR. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) with a viral vector at an MOI of no more than 10, no more than 20, no more than 30, no more than 40, no more than 50, no more than 60, no more than 70, no more than 80, no more than 90, no more than 100, no more than 150, no more than 200, no more than 250, no more than 300, no more than 350, no more than 400, no more than 450, no more than 500, no more than 600, no more than 700, no more than 800, no more than 900, or no more than 1000 in a method of the invention to modify at least 70% of treated cells to successfully express a CAR. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) with a viral vector at an MOI of no more than 10, no more than 20, no more than 30, no more than 40, no more than 50, no more than 60, no more than 70, no more than 80, no more than 90, no more than 100, no more than 150, no more than 200, no more than 250, no more than 300, no more than 350, no more than 400, no more than 450, no more than 500, no more than 600, no more than 700, no more than 800, no more than 900, or no more than 1000 in a method of the invention to modify at least 80% of treated cells to successfully express a CAR. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) with a viral vector at an MOI of no more than 10, no more than 20, no more than 30, no more than 40, no more than 50, no more than 60, no more than 70, no more than 80, no more than 90, no more than 100, no more than 150, no more than 200, no more than 250, no more than 300, no more than 350, no more than 400, no more than 450, no more than 500, no more than 600, no more than 700, no more than 800, no more than 900, or no more than 1000 in a method of the invention to modify at least 85% of treated cells to express a CAR. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) using a viral vector at an MOI of no more than 10, no more than 20, no more than 30, no more than 40, no more than 50, no more than 60, no more than 70, no more than 80, no more than 90, no more than 100, no more than 150, no more than 200, no more than 250, no more than 300, no more than 350, no more than 400, no more than 450, no more than 500, no more than 600, no more than 700, no more than 800, no more than 900, or no more than 1000. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) using a viral vector at an MOI of between approximately 10 and approximately 1000, approximately 10 and approximately 500, approximately 10 and approximately 300, or of between approximately 10 and approximately 100. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) using a viral vector at an MOI of between approximately 100 and approximately 1000, approximately 100 and approximately 500, approximately 10 and approximately 300, or of between approximately 10 and approximately 200. In a suitable embodiment of a method of the invention, transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®) with a viral vector at an MOI of approximately 100 to modify at least 85% of treated cells to express a CAR. The embodiments of the methods of the invention using a combination of Poloxamer F108 and polybrene (such as Lentiboost®) discussed above may advantageously be employed with a CMV vector comprising a nucleic acid encoding the chosen CAR. Granulocyte progenitor cells A “granulocyte progenitor cell”, as used herein, may be a cell more differentiated than an HSC but less differentiated than a granulocyte precursor cell. 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”. Methods of preparing cells for therapeutic use The invention provides methods of preparing cells, modified to express a CAR, for therapeutic use. Methods of the invention may employ stem cells, which undergo expansion to produce a population of granulocyte progenitor cells, and / or granulocyte progenitor cells that undergo differentiation into granulocytes, or precursors thereof. 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 and cell culture conditions are set out further below. Existing in vitro methods for producing granulocytes (e.g. neutrophils) and precursors thereof suffer certain limitations including the production of low yield of granulocytes (e.g. neutrophils) and precursors thereof, 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). 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 invention. These include useful embodiments of the stem cells 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 precursor cells) produced by the methods of the invention are considered in more detail elsewhere in the specification. The thirteenth aspect of the invention provides a preferred method of preparing cells for therapeutic use. This method, referred to as v0.4 protocol comprises culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells; and modifying the cells to express a CAR. This is referred to herein as the “v0.4” protocol referred to herein. In such a method, the expansion step 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”. Details of methods that may be used to produce granulocyte precursor cells suitable to be employed as cells of the invention are set out in Figure 13, which provides details of the exemplary protocols “v0.3c”, “v0.4c” and “v0.4d”. The method of obtaining a granulocyte precursor cell may comprise: 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 progenitor 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; 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 granulocyte precursor cells, the cell culture conditions comprising the presence of: • a basal medium; • SCF; • TPO; and • G-CSF. The following paragraphs provide guidance as to certain embodiments that may be used in respect of the culture conditions employed in the methods of obtaining a granulocyte precursor cell. 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. The expansion medium may comprise Iscove’s Modified Dulbecco’s Medium (IMDM). The expansion step may last from day E0 to day E8. The expansion steps employ required cytokines, and may further employ optional cytokines, as discussed further below. Methods of the invention comprising an expansion step may utilise cell culture condition in which stem cell factor (SCF), FLT-3 ligand (FLT3-L) and thrombopoietic (TPO) are all present. SCF may be provided at a concentration of approximately 0.01-10 µg / ml. SCF may be provided at a concentration of approximately 0.05-0.3 µg / ml. SCF may be provided at a concentration of approximately 0.1-0.2 µg / ml. FLT-3 ligand may be provided at a concentration of approximately 0.01-10 µg / ml. FLT-3 ligand may be provided at a concentration of approximately 0.05-0.3 µg / ml. FLT-3 ligand may be provided at a concentration of approximately 0.1-0.2 µg / ml. TPO may be provided at a concentration of approximately 0.001-0.2 µg / ml. TPO may be provided at a concentration of approximately 0.005-0.03 µg / ml. TPO may be provided at a concentration of approximately 0.01-0.02 µg / ml. 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 (e.g., the “v0.4d” protocol). The expansion medium may comprise insulin-transferrin-selenium (ITS) and / or human serum albumin (HSA). The HSA may be recombinant HSA. HSA may be provided at a weight / volume (w / v) concentration of approximately 0.1% – 5%. For example, HAS may be provided as a supplement may be provided at a concentration of approximately 1%. On the first day of expansion the medium to be used to generate progenitor cells may comprise 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). On the first day of expansion the medium may comprise 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). On the first day of expansion the medium to be used in a method in accordance with the first aspect of the invention may comprise 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). On the first day of expansion, the medium to be used may comprise 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). 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. UM171 represents a favoured example of a pyrimido-[4,5-b]-indole derivative that may be used in the methods of the invention. 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. The pyrimido-[4,5-b]-indole derivative may be 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. The pyrimido-[4,5-b]-indole derivative may 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. The pyrimido-[4,5-b]-indole derivative may be UM171 and may be provided to the cells during expansion in four incidences. Suitably these incidences may be at E0, E4, E6 and E8. In one 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 may be provided to the cells during expansion in three incidences at E0, E4, and E6. In one 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. The pyrimido-[4,5-b]-indole derivative may be UM729, which is provided to the cells during expansion in three incidences at E0, E4, and E6. The pyrimido-[4,5-b]-indole derivative may be UM729 and may be 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%. Methods of the invention may comprise a differentiation step, in which cells are cultured in conditions the promote differentiation of a population of progenitor cells into a population of granulocyte precursor cells. Suitably the granulocyte precursor cells produced may be cells characterised with reference to the marker or gene expression profiled disclosed in respect of any of the first to fifth aspects of the invention. In a suitable embodiment, a differentiation step lasts from day D0 to day D4. In a method comprising an expansion step, E8 of the expansion step may correspond to D0 of the differentiation step. 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 one embodiment, the basal medium is not IMDM. In a suitable embodiment of a differentiation step 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 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 may 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 may 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 may make 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 may 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. The products of such differentiation steps may be granulocyte precursors suitable to be employed in any of the first to fifth or first to sixth aspects of the invention. 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 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). Further sources of natural stem cells, 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. In a suitable embodiment a population of granulocytes, or precursors thereof (e.g., granulocyte precursor 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 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 is obtainable (e.g. obtained) by a method of the present invention. Stem cells suitable for use in the methods of the invention may be selected on the basis of the cytocidal activity of a donor’s cells. Suitable ways in which CKA may be calculated have been described above. More detail of a suitable method is set out in Example 15. Suitably, such a screening procedure may be employed as an optional preliminary step in a method of the invention, such as a method employing the v0.3 (v0.3c) or v0.4 (optionally v0.4c or v0.4d) protocols disclosed herein. Thus, in a suitable embodiment, a granulocyte precursor cell, or cell population, in accordance with the invention has been derived from a donor having a granulocyte (neutrophil) with high CKA. Further, in a suitable embodiment, the population of stem cells employed in a method of the invention, such as a method of the thirteenth of fourteenth aspect of the invention, has been derived from a donor having a granulocyte (neutrophil) with high CKA. Progenitor cells suitable for use in the methods of the invention The methods of third aspect of the invention make use of populations of progenitor cells as the “starting material” from which granulocytes 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 to produce a population of progenitor cells. Progenitor cells, and populations of 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. Except for where the context requires otherwise, they should be considered appliable to progenitor cells as referred to in any embodiment of the invention. In a suitable embodiment, a population of progenitor cells suitable for use in the method of the invention, or that may be produced by the methods of the invention may comprise Suitably in a population of progenitor 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 • 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: • 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: • 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 between 10% and 40% of the cells of the population express CD45RA Methods in accordance with the thirteenth aspects of the invention The thirteenth aspect of the invention provides a method of preparing cells for therapeutic use, the method comprising culturing a population of stem cells in cell culture conditions to produce a population of progenitor cells, wherein the cell culture conditions for producing the progenitor 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; and • modifying the cells to express a CAR. This thirteenth aspect of the invention is a preferred method for the manufacture of populations of cells of the invention, in particular populations of cells of the first to fifth aspects of the invention. The number of cells may increase during this period of cell culture. Accordingly, the period of culturing a population of stem cells in cell culture conditions to produce a population of 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. The number of 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 present at the start of the cell culture. Indeed, the number of 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 present at the start of the cell culture. A method in accordance with the thirteenth 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). 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 further comprise: • ITS; and / or • HSA. In a suitable embodiment the cell culture conditions for producing the progenitor cells 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 further comprise: • IL-3; and / or • IL-6. By way of example, the cell culture conditions for producing the 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 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 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 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. 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. 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 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. A method in accordance with the thirteenth aspect of the invention may, further comprise a step of culturing the progenitor cells to promote their differentiation into granulocytes, or granulocyte precursor cells. Such a method may comprise culturing a population of progenitor cells in cell culture conditions that promote differentiation of the progenitor cells into granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) 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 to granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) used in these methods of the third aspect of the invention, may be referred to as a “differentiation phase” or “differentiation step”. In a suitable embodiment, 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 progenitors into granulocytes, or precursors thereof. 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, 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, 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 into granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) 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 into granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) 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 into granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprise each of 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 into granulocytes, or precursors thereof. 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 into granulocytes, or precursors thereof. 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. A method employing such a differentiation step 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. Modification of cells to express a CAR may occur before the expansion phase, during the expansion phase, before the differentiation phase, during the differentiation phase, or after the differentiation phase. As set out in the Examples, modification of cells to express a CAR during the expansion phase may be preferred. Expression of markers within cell populations of the invention The first, third, fourth and fifth 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 second 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 third, fourth and fifth 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). 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. 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 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. HLA-DR 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. A suitable embodiment of the second aspect of the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) 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 suitable embodiment of the second aspect of the invention provides a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) 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. Gene expression markers within cells, or cell populations, of the invention As set out above, a granulocyte precursor cell of the first aspect of the invention, or a granulocyte precursor cell present in a population of cells of the first, second, third, fourth or fifth aspects of the invention, 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; and / or • 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. 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: 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- 3921 / 11 / 11 / 2302). 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 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: 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: https: / / academic.oup.com / jleukbio / article- Without wishing to be bound by any 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: abstract / 80 / 1 / 196 / 6922777?redirectedFrom=fulltext). Without wishing to be bound by any theories, although the significance of low expression 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 1: 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 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. Preferably, the granulocyte precursor cell is a promyelocyte, a myelocyte, or an intermediate thereof or a cell resembling an in vivo differentiated 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 Distinct gene marker profile: A population of granulocyte precursor cells particularly useful as cells of the invention 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, these granulocyte precursor cells 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 these granulocyte precursor cells. 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), 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. The presence of a gene marker profile of this sort within cells, for example within granulocyte precursor cells of the invention, or population of such cells, may be determined by use of any suitable technique. A suitable example of such a technique is set out in Example 14 (“Bulk RNA-sequencing analysis”). Cytocidal activity of cells or pharmaceutical compositions of the invention Cytocidal activity of cells or cell populations of the invention, or of pharmaceutical compositions of the invention, may be determined by means of a suitable cell killing assay. In a suitable embodiment, a cell killing assay mixes “effector cells” (cells of the invention or appropriate control cells) with “target cells” of the sort it is wished to be killed. The target cells may, for example, be cancer cells, or cells infected with a pathogen. Additional cell types (such as PBMCs, representing the cells of a subject’s immune system) may also be included in the mixtures, as desired. Cytocidal activity may be assessed by mixing the effector cells and target cells (for example at a known ratio) and incubating the mixture for a required period of time. The number of target cells present at the end of the incubation period allows the proportion of target cells that has been killed during the incubation period to be determined. This may be expressed as percentage cytocidal activity (e.g. percentage cancer killing activity), or as percentage lysis. A cancer cell to be used as a target cell in such an assay may be one or more selected from a pancreatic cancer cell line, a liver cancer cell line, an oesophageal cancer cell line, a stomach cancer cell line, a cervical cancer cell line, an ovarian cancer cell line, a lung cancer cell line, a bladder cancer cell line, a kidney cancer cell line, a brain cancer cell line, a prostate cancer cell line, a myeloma cancer cell line, a non-Hodgkin’s lymphoma (NHL) cell line, a larynx cancer cell line, a uterine cancer cell line, or a breast cancer cell line. Suitable cell lines are available commercially from the American Type Culture Collection United Kingdom (U.K.), Guernsey, Ireland, Jersey and Liechtenstein, LGC Standards, Queens Road, Teddington, Middlesex, TW110LY, UK. For example, a pancreatic cell line may be one or more of Capan-2, ATCC HTB-80; Panc 10.05, ATCC CRL-2547; CFPAC-1, ATCC CRL-1918; HPAF-II, ATCC CRL-1997; SW 1990, ATCC CRL-2172; BxPC-3, ATCC CRL-1687; AsPC-1, ATCC CRL-1682; ATCC® TCP-1026™; SW1990, ATCC CRL-2172; SU.86.86, ATCC CRL- 1837; BXPC-3, ATCC CRL-1687; Panc 10.05, ATCC CRL-2547; MIA-PaCa-2, ATCC CRL- 1420; PANC-1, ATCC CRL-1469; or ATCC® TCP-2060™. Preferably the cancer cell line is pancreatic cancer cell line, such as PANC-1. In a suitable embodiment the cancer cell line is a cervical cancer cell line, such as a HeLa cell. The incubation step may be carried out for between 1 hour and 100 hours. Suitably, the incubation step may be carried out for between 5 hours and 75 hours, for example between 10 hours and 20 hours. The incubation step may be carried out for between 6 hours to 6 days. Suitably, the incubation step may be carried out for between 6 hours and 2 days, for example for between 12 hours to 36 hours, such as between 16 to 24 hours. In a suitable embodiment the incubation step is carried out for 24 hours. In another embodiment the incubation step is carried out for 48 hours. The incubation step may be carried out at any temperature suitable for cell growth and viability, for example at a temperature between 35 °C to 42 °C, suitably at 37 or 39 °C. Preferably the incubation step is carried out at 37 or 39 °C for 24 hours. Preferably the incubation step is carried out for 16-24 hours at 30-40 °C (e.g.37°C). The percentage of target cells killed can be measured by reference to the total number of starting target cells. The number of target cells killed can be measured using any suitable means, for example by viability staining (e.g. trypan blue staining), and microscopy, or using other automated means, for example by cell electronic sensing equipment, such as the RT- CES™ system available from ACEA Biosciences, Inc. (11585 Sorrento Valley Rd., Suite 103, San Diego, CA 92121, USA). In some embodiments the percentage of target cells killed may be determined within 24 hours (e.g. of incubating a target cell and a cell of the invention). The percentage of cancer cells killed is preferably the maximum number of cancer cells killed when carrying out such an assay. The percentage of cancer cells killed in said admixture may be the maximum percentage of cancer cells killed within 48 hours of forming the admixture. Suitably the effector cells and target cells may be used in such an experimental model at a ratio of 1 (or more):1, of 1.5 (or more):1, of 2 (or more):1, of 2.5 (or more):1, of 3 (or more):1, or 3.5 (or more):1, of 4 (or more):1, of 4.5 (or more):1, of 5 (or more):1, of 5.5 (or more):1, of 6 (or more):1, of 6.5 (or more):1, of 7 (or more):1, of 7.5 (or more):1, of 8 (or more):1, of 8.5 (or more):1, of 9 (or more):1, of 9.5 (or more):1, or of 10 (or more):1. Suitably the effector cells and target cells may be used in such an experimental model at a ratio of 11 (or more):1, of 12 (or more):1, of 13 (or more):1, of 14 (or more):1, or of 15 (or more):1. For example, the effector cells and target cells may be used in such an experimental model at a ratio of 20 (or more):1, of 25 (or more):1, of 30 (or more):1, of 35 (or more):1, of 40 (or more):1, or 45 (or more):1, or of 50 (or more):1. Suitably, effector cells and target cells may be used in such an experimental model at a ratio of 60 (or more):1, of 70 (or more):1, of 80(or more):1, of 90 (or more):1, or of 100 (or more):1. In a suitable embodiment, a population of cells of the invention, or a pharmaceutical composition of the invention, has cytocidal activity that is increased by at least 2.5-fold as compared to a control cell population. In a suitable embodiment, a population of cells of the invention, or a pharmaceutical composition of the invention, has cytocidal activity that is increased by at least 3 fold, at least 3.5 fold, at least 4 fold, at least 4.5 fold, at least 5 fold, at least 5.5 fold, at least 6 fold, at least 6.5 fold, at least 7 fold, at least 7.5 fold, or at least 8 fold as compared to a control cell population. For example, a population of cells of the invention, or a pharmaceutical composition of the invention, may have cytocidal activity that is increased by at least 9 fold, at least 10 fold, at least 11 fold, at least 12 fold, at least 13 fold, at least 14 fold, or at least 15 fold, as compared to a suitable control cell population. Indeed, a population of cells of the invention, or a pharmaceutical composition of the invention, may have cytocidal activity that is increased by at least 20 fold, at least 25 fold, at least 30 fold, at least 35 fold, at least 40 fold, at least 45 fold, or at least 50 fold, or more, as compared to a suitable control cell population. Suitably, a population of cells of the invention, or a pharmaceutical composition of the invention, has cytocidal activity that is increased approximately 3 fold, approximately 4 fold, approximately 5 fold, approximately 6 fold, approximately 7 fold, approximately 8 fold, approximately 9 fold, approximately 10 fold, approximately 11 fold, approximately 12 fold, approximately 13 fold, approximately 14 fold, approximately 14 fold, approximately 16 fold approximately 17 fold, approximately 18 fold, approximately19 fold, or approximately 20 fold. Suitably a control cell population is selected from the group consisting of: a population of granulocytes or precursors thereof having the marker profile recited in claim 1, that do not comprise a CAR; and a population of unmodified granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) from a subject. The subject may be selected from the group consisting of: a healthy subject, and a cancer patient subject. In a suitable embodiment a population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to kill at least 5% of target cells in a method described herein. A population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to kill at least 10%, 20%, 30%, 40%, 50%, or 51.5% of the target cells present. In a suitable embodiment a population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to kill at least 60% of the target cells present. In a suitable embodiment a population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to kill at least 70% of the target cells present. For example, a population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to at least 80% or 90% of the target cells present. In a particularly preferred embodiment, a population of cells of the invention, or pharmaceutical composition of the invention, may have the ability to kill at least 51.5% of the target cells present. Pharmaceutical compositions of the invention The seventh 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 first to sixth 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. 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 granulocytes, or precursors thereof (e.g., granulocyte precursor cells)) 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, infection or autoimmune disease). 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. Medical uses and methods of treatment of the invention As set out above, populations of 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 that can be used therapeutically. Cells of the invention may exert immunomodulatory activity 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 and pharmaceutical compositions of the invention may be used in the treatment of cancer, infections, or autoimmune diseases. 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 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 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 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. 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 granulocytes or precursors thereof produced by alternative means. Suitably, a cell of the invention, or population of 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, 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. 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 further 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 other adoptive immunotherapy cells. Suitably, the further adoptive immunotherapy cell also expresses a chimeric antigen receptor (CAR). Such a further adoptive immunotherapy cell may be a CAR-T cell. These combined uses with further 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 a further adoptive immunotherapy cell. A pharmaceutical composition, or population of cells, of the invention may be used in combination therapy with a further adoptive immunotherapy cell expressing a CAR specific for a TAA as described above. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing therapeutic activity of the further adoptive immunotherapy cell. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing activation of the further 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 further adoptive immunotherapy cell. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing accumulation of further adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing proliferation of the further adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing persistence of the further adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing survival of the further adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by increasing cytotoxic activity of the further adoptive immunotherapy cells. Suitably, the pharmaceutical composition, or population of cells, may achieve a therapeutic effect by decreasing T cell exhaustion of further 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 further 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 further 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 further 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 further adoptive immunotherapy cells. In a suitable embodiment, cells of the invention, such as in a pharmaceutical composition of the invention, are provided after the further 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 further 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 further 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. 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 cancer may be a primary cancer. Suitably the cancer may be a metastatic cancer. In such an embodiment, the cells of the invention may express a CAR specific to an antigen, such as a TAA, relevant to the cancer in question. 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: cervical cancer, head and neck cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach 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 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: a cervical cancer, such as a metastatic cervical cancer; and head and neck 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. In such an embodiment, the cells of the invention may express a CAR specific to a pathogen associated antigen relevant to the infection in question. 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. Treatment of 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. In such an embodiment, the cells of the invention may express a CAR specific to an antigen associated with the 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. A suitable CAR may be selected accordingly. 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 eleventh 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 granulocytes, or precursors thereof (e.g., granulocyte precursor cells)” includes a plurality of such populations and reference to “the population of granulocytes, or precursors thereof (e.g., granulocyte precursor cells)” includes reference to one or more populations of granulocytes, or precursors thereof (e.g., granulocyte precursor cells) and equivalents thereof known to those skilled in the art, and so forth. The term “one or more” as used herein may mean at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, or 20, etc. In one embodiment, wherein “one or more” precedes a list, “one or more” may mean all of the members of the list. Similarly, the term “at least one” as used herein may mean at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, or 20, etc. In one embodiment, wherein “at least one” precedes a list, “at least one” may mean all of the members of the list. 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. BRIEF DESCRIPTION OF THE DRAWINGS Figure 1: Flow cytometry data for three donors: NTP7 (Figure 1A), NTP8 (Figure 1B), and NTP9 (Figure 1C) showing the expression of CARs in granulocytic cells of the invention as a percentage of the parent (%P) gate, which is a percentage of the live cell population. Results are discussed in Example 1. Figure 2: Percentage of transduced granulocytic cells of the invention (%VE+) detectable over a prolonged culture period up to 13 days across three donors. Results of the study are set out in Example 2. Figure 3: Flow cytometry data showing the expression of CARs in a population when the granulocytic cells of the invention underwent a mock transduction. Results are set out in Example 3. Figure 4: Flow cytometry data showing the effect of Nevirapine, an HIV anti-viral medication that blocks the delivery of viral vector, on the success of the transduction process that leads to the cellular expression of CARs in granulocytic cells of the invention. Results of this study are set out in Example 4. Figure 5: The total cell counts for donor NTP5 (Figure 5A) and donor NTP6 (Figure 5B) are shown for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and granulocytic cells of the invention transduced during expansion (CAR), over the expansion period (E1 – E8), and through differentiation (E8 – E8D5). Figure 5C shows the transduction efficiency for two donors – NTP5 and NTP6 – assessed on harvesting. Results of this study are set out in Example 5. Figure 6: Percentage cell lysis of A549 cancer cells at effector:target (E:T) ratios of 1.2:1, 2.5:1, 5:1, 10:1, and 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and granulocytic cells of the invention transduced during expansion (CAR-4D5) when tested directly post-thaw for two donors: NTP5 (Figure 6A), and NTP6 (Figure 6B). Results of this study are discussed in Example 6. Figure 7: Percentage cell lysis of A549-HER2hi cancer cells at effector:target (E:T) ratios of 1.2:1, 2.5:1, 5:1, 10:1, and 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and granulocytic cells of the invention transduced during expansion (CAR-4D5) when tested directly post-thaw for two donors: NTP5 (Figure 7A), and NTP6 (Figure 7B). Results of this study are set out in Example 7. Figure 8: Percentage cell lysis of A549 cancer cells at effector:target (E:T) ratios of 1.2:1, 5:1, and 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and granulocytic cells of the invention that were transduced during differentiation (CAR-4D5) when tested post-thaw with a two day maturation period for two donors: NTP5 (Figure 8A), and NTP6 (Figure 8B). Results of this study are set out in Example 8. Figure 9: Percentage cell lysis of A549 cancer cells at effector:target (E:T) ratios of 1.2:1, 5:1, and 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and cells expressing CARs that were transduced during expansion (CAR-4D5) when tested post- thaw with a two day maturation period for two donors: NTP5 (Figure 9A), and NTP6 (Figure 9B). Figures 9C and 9D show the results of a study conducted under the same conditions as above, but instead on A549HER2hi cancer cells. Results of this study are set out in Example 9. Figure 10: Percentage cell lysis of SK-BR-3 cancer cells at effector:target (E:T) ratios of 1.2:1, 5:1, and 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and cells expressing CARs that were transduced during expansion (CAR-4D5) when tested post-thaw with a two day maturation period for two donors: NTP5 (Figure 10A), and NTP6 (Figure 10B). Results of this study are set out in Example 10. Figure 11: Percentage cell lysis of A549HER2hi cancer cells at an effector:target ratio of 20:1 for 3 experimental groups: untransduced cells (UTD), mock transduced (‘mock’), and cells expressing CARs that were transduced during expansion (CAR-4D5) with viral vectors encoding two different promoters (PGK, miR223) and the HER2.CAR.CD3z transgene promoter. Expansion conditions comprised the pyrimido-[4,5-b]-indole derivative - UM171 - and the cytokines SCF, FLT-3L and TPO. Results of this study are set out in Example 11. Figure 12: Percentage cell lysis of A549HER2hi cancer cells at an effector:target ratio of 20:1 using cancer patient neutrophils, and granulocytic cells of the invention expressing a CAR (designated “CAR-IMAN”). Results are discussed in Example 12. Figure 13: 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 14: Results of the study set out in Example 13, comparing proportion of cells expressing CARs and intensity of CAR expression at different MOIs of viral vector for the different experimental transduction protocols used in the study. Figure 15: Results of the study set out in Example 13, comparing proportion of cells expressing CARs and intensity of CAR expression over time, in respect of the different experimental transduction protocols used in the study. Figure 16: 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. EXAMPLES The following Examples make use of untransduced granulocytic cells (designated “UTD” in Figures), and mock transduced granulocytic cells (designated as “mock”) as controls. The same granulocytic cells were transduced with a CAR-expressing vector, to give rise to granulocytic cells of the invention. Donors used were referred to as NTP5, NTP6, NTP7, NTP8, NTP9, NTP015. The cancer cells used in the cytocidal assays were of the A549 cell line or the SK-BR3 cell line. In some experiments, the A549 cell line was genetically engineered to over-express HER2; these cells are referred to as A549-HER2hi. As set out below, a range of Effector:Target (E:T) cell ratios, i.e. the number of granulocytic cells:the number of cancer cells (whether A549, A549HER2hi, or SK-BR-3), were investigated. Those that were found to be the most effective in respect of granulocytic cells of the invention, and which are further discussed herein, were ratios of 5:1 and above (i.e. in which 5 or more granulocytic cells are present per cancer cell). The granulocytic cells of the invention utilised in Example 11 were produced by a method involving an expansion step in the presence of the pyrimido-[4,5-b]-indole derivative UM171 (v0.4 protocol – thirteenth aspect of the invention). Granulocytic cells of the invention in the other Examples were prepared using an expansion step that lacked this agent (v0.3 protocol – fourteenth aspect of the invention). Example 1: CD34+ cells from all donors tested underwent successful transduction to express CARs Method: CD34+ cells from 3 donors - NTP7, NTP8, and NTP9 - were thawed and cultured in IMDM+1%HSA and 1x ITS (insulin transferrin selenium). The media was supplemented with SCF (200ng / ml), FLT3L (200ng / ml), TPO (20ng / ml), IL-3 (15 ng / ml), IL-6 (15 ng / ml). On day 4, 12ul virus encoding CAR.CD3z (VSVg-LV) was added on to wells of a 24 well plate which had been precoated overnight with r-fibronectin (20ug / ml). The plate was centrifuged for 1h at 2000g and 32°C. The viral vector was then removed and 1.5E5 cells were added on to each well. The cells were spinoculated onto the virus-coated well and then incubated for 4 days. Flow cytometry for CAR expression was performed on day 7 post-thaw (4 days post- spinoculation). The results are set out in Figure 1. They show that CD34+ cells can be effectively transduced with a CAR-expressing vector during culture conditions in which expansion of the cell population occurs. Furthermore, this experimental method was effective across cells from multiple donors at a broadly similar level of efficacy, from 27 – 40%. Example 2: Transduced cells are detectable after prolonged cell culture CD34+ cells from 3 donors – NTP6, NTP7, and NTP9 - were thawed and cultured as per the method of Example 1 up to the spinoculation onto the virus-coated well and 4 days incubation. Flow cytometry for CAR expression was performed on day 7 post thaw (4 days post spinoculation). On day 7 the cells were replenished in differentiation media (SCF, TPO, GCSF, each at 130ng / ml). Flow cytometry for CAR expression was performed on days 11 and 13. The results (set out in Figure 2) show that transduced cells from all donors investigated can successfully be detected after a prolonged period in culture across. Example 3: Cells that underwent mock transduction had very low % CAR expression CD34+ cells were thawed and cultured in IMDM supplemented with 1%HSA, 1x ITS (insulin transferrin selenium). The media was supplemented with SCF (200ng / ml), FLT3L (200ng / ml), TPO (20ng / ml), IL-3 (15 ng / ml), and IL-6 (15 ng / ml). On day 4, cells were transduced in a GREX24 with Hank’s Balanced Salt Solution (HBSS) and vectofusin-1 as a transduction enhancer, in a final volume of 2 ml. The following day 4 ml of media (of the formulation described above) was added. On day 8 a sample of cells was taken for flow cytometry to assess GFP and CAR expression. The results are shown in Figure 3. They demonstrate that only 0.05% of the cells tested were positive for CARs, a result within margins for background labelling, thus demonstrating the success of the mock transduction process.

[0002] Example 4: Transduction approach does not lead to pseudotransduction CD34+ cells were thawed and cultured in IMDM supplemented with 1%HSA, 1x ITS (insulin transferrin selenium). SCF (200ng / ml), FLT3L (200ng / ml), TPO (20ng / ml), IL-3 (15 ng / ml), IL- 6 (15 ng / ml). On day 4, cells were transduced in a GREX24 at an MOI of 250 using HER2- CAR vector (MOI 100 for GFP) with vectofusin-1 as a transduction enhancer, in a final volume of 2 ml. Nevirapine was added to a final concentration of 1mM. The following day, 4 ml of media (of the formulation described above) was added. On day 8, a sample of cells was taken for flow cytometry to assess GFP and CAR expression. Results are shown in Figure 4. Nevirapine leads to a blockage of viral entry into cells. In the nevirapine negative (-Nevirapine) group, 17.43% of the cells were CAR+. This reduced to 1.75% CAR+ on the introduction of nevirapine in the medium. This corresponds to a 90% reduction in CAR+ expression when the virus was blocked, which provides evidence that the virus is indeed penetrating cells and resulting in the expression of CARs in granulocytic cells. The data therefore shows that the CAR expression is ‘true’ transduction and not due to episomal expression of the viral genome. Example 5: The addition of CARs to granulocytic cells does not impact cell viability compared to untransduced or mock transduced granulocytic cells Method: On expansion day 0 (E0), CD34+ material was thawed and seeded into a GREX6M in 10 ml of expansion media (IMDM supplemented with 1%HSA, 1x ITS (insulin transferrin selenium),SCF (200ng / ml), FLT3L (200ng / ml), TPO (20ng / ml), IL-3 (15 ng / ml), IL-6 (15 ng / ml). A non-TC coated 96wp was filled with 0.1 ml 20ug / ml r-fibronectin solution, in PBS. Results are shown in Figure 5. On expansion day 1 (E1), the wells of the 96wp were washed with 0.1ml of PBS and 100ul of viral vector (CAR.4D5.CD3z) was added in to each well of the plate (20 wells: 10wells for each donor). To the mock wells an equivalent volume of HBSS was added. The plates were centrifuged for 2h at 2000 x g at 32°C. The cells in the GREX were resuspended, counted and adjusted to 1E6 / ml by centrifuging and removing media. After viral preloading the virus was discarded and 100ul of cells (1e5) was added to each well of the 96wp (10 wells / condition / donor). The plate was centrifuged for 10min at 400g at 32C. The plate was placed in the incubator overnight. For the untransduced condition, 1E6 cells were placed in GREX6M and topped up to 40ml with expansion media (UTD condition), before placing back in the incubator. On expansion day 2 (E2): The cells from each condition / donor of the 96wp were resuspended and transferred to one well of the GREX6M and topped up to 40ml of expansion media. On expansion day 4 (E4): Media from each well was aspirated to leave approximately 5ml and cells were resuspended and counted using the NC250. A sample was taken for flow cytometry. The wells were topped up to 50ml with fresh expansion media. On expansion day 6 (E6): The cells were resuspended and counted using the NC250 and a sample was taken for flow cytometry. 50ml of expansion media was added to each well (final volume 100ml). On expansion day 8 (E8): Media was each well of the GREX6M was aspirated to leave approximately 5ml. The cells were resuspended and counted using the NC250 and a sample was taken for flow cytometry. The wells were topped up to 50ml with differentiation media (IMDM 2%HSA, 1x ITS with ,SCF, TPO, GCSF (all at 130ng / ml). The 8-day long cell expansion phase was then followed by a 5-day long differentiation phase. On day 3 of the differentiation phase (E8D3), the cells were resuspended and counted using the NC250 and a sample was taken for flow cytometry.50ml of differentiation media (+GM- CSF, 10ng / ml final concentration) was added to each well (final volume 100ml). On day 4 of the differentiation phase (E8D4), TNF alpha (TNFa) was added to each well to a final concentration of 1 ng / ml. On day 5 of the differentiation phase (E8D5): Media was each well of the GREX6M was aspirated to leave approximately 30ml. The cells were resuspended and counted using the NC250. A sample was taken for flow cytometry. The cells were cryopreserved in CS10 at 20E6 / vial. The results show that the cell count was comparable across the untransduced, mock transduced (‘mock’), and the CAR+ transduced (‘CAR’) cells at multiple time points: E1, E4, E6, E8D3, and E8D5 for donor NTP5. There was a slight drop in the untransduced cell count for NTP6 at E8D3, but by E8D5 this recovered to similar numbers as the other experimental groups. In addition, the transduction efficiency of the granulocytic cells of the invention was above 25% across both donors. Example 6 – Granulocytic cells of the invention show up to 7-fold increased cytocidal activity of over untransduced or mock transduced granulocytic cells in A549 cells when tested directly post-thaw A549 cells were seeded into a white 96 well-plate (1E4 / well). The following day the granulocytic cells of the invention generated as per the method of Example 5 were thawed and resuspended in DMEM10 and seeded onto the target A549 cells at the shown E:T ratios. Lysis was measured after 2 days by the addition of ONEGlo reagent and comparing the luminescence from sample wells to target alone wells. The results are shown in Figure 6. While low cytotoxicity was observed following cryopreservation, though the granulocytic cells of the invention did perform consistently better across both donors and target cell lines. Example 7 – Granulocytic cells of the invention show increased cytocidal activity over untransduced or mock transduced granulocytic cells of A549HER2hi cells when tested directly post-thaw A549 HER2hi cells were seeded into a white 96 well-plate (1E4 / well). The following day the granulocytic cells of the invention generated as per the method of Example 5 were thawed and resuspended in DMEM10 and seeded onto the target cells at the shown E:T ratios. Lysis was measured after 2 days by the addition of ONEGlo reagent and comparing the luminescence from sample wells to target alone wells. Results are shown in Figure 7. Generally low cytotoxicity was observed following cryopreservation in the control groups, though the granulocytic cells of the invention did perform consistently better across both donors and target cell lines. The cells were genetically engineered to over-express HER2, as it was known that A549 cells in general only express conservative quantities of the gene. By inducing over-expression, the A549-HER2hi cells were more likely to mimic the cells for which the granulocytic cells of the invention were designed to target. This change in the expression of the HER2 marker did not cause an observable increase the cytocidal activity over the previous example in A549 cells. The directly post-thaw condition was suboptimal and adversely impacted the efficacy of the granulocytic cells of the invention. Furthermore, on a theoretical level, this condition would not be a closely aligned method for assessing cytocidal activity as per the inventor’s intended use of the therapy. As the cells are intended to be injected into a patient, this data constitutes a preliminary assessment of the cytocidal activity prior to the expected maturation that would occur once the cells were delivered in vivo. This hypothesis led to the studies shown in the subsequent examples, wherein cells were subjected to two days of post-thaw maturation prior to the assessment of cytocidal capability. Example 8 – Granulocytic cells of the invention show increased cytocidal activity of up to 4-fold over untransduced or mock transduced granulocytic cells when transduced during differentiation and with 2 days post-thaw maturation CD34+ cells from donors NTP5 and NTP6 were thawed and cultured in IMDM supplemented with 1%HSA, 1x ITS (insulin transferrin selenium). SCF (200ng / ml), FLT3L (200ng / ml), TPO (20ng / ml), IL-3 (15 ng / ml), IL-6 (15 ng / ml). On E4, 5E6 cells were seeded into 50ml of media (of the formulation described above). 45ml of media was removed on E8 and 50ml of differentiation media was added (SCF, TPO, and GCSF, each at 130ng / ml). On E8D3, wells of a non-tissue culture (non-TC) coated 24 well plate were coated with 0.5ml 20µg / ml retronectin solution, in PBS for 1h at 37°C. The wells were washed with 1ml of PBS and 400µl of viral vector (CAR.4D5.CD3z or HBSS for mock) was added to 10 wells of the 24 well plate (5 wells each for NTP5 and NTP6). The plates were centrifuged for 2h at 2000 g at 32°C. For transduction, 5E6 cells were taken from well 2 of each donor and centrifuged. The media was aspirated and 5ml of the media was added (differentiation media+ GMCSF at 10ng / ml). 1ml (1E6) of cells from each donor was added to 5 wells of virus coated wells and mock coated plates. The plate was centrifuged for 10 min at 400g at 32°C. After centrifugation the plates were kept in an incubator overnight. On E8D4, the cells were resuspended using a 1ml pipette and all 5 wells from each condition / donor were pooled into 1 well of a GREX24 well plate. TNFa was added to each GREX well to a final concentration of 1 ng / ml. On E8D5, cells were cryopreserved. Cells were thawed into IMDM 2%HSA, 1x ITS with SCF, TPO, GCSF (all at 130ng / ml), GM- CSF (10ng / ml) and TNFa 1ng / ml) within a GREX24. Two days post thaw A549 cells were seeded into a white 96 well plate (1E4 / well). The following day the granulocytic cells of the invention were resuspended in DMEM10 and seeded onto the target cells at the shown E:T ratios. Lysis was measured after 2 days by the addition of ONEGlo reagent and comparing the luminescence from sample wells to target alone wells. Results are shown in Figure 8. As a proof-of-concept preliminary study, the transduction was carried out during differentiation, on E8D3. It was found that the granulocytic cells of the invention of donor NTP5 were capable of increasing the %lysis at an E:T ratio of 5:1 in the cells by over 4-fold. For the higher E:T ratio, a doubling was generally observed across both donors. This study showed a high degree of consistency in the granulocytic cells of the invention, with an average of 26% versus 27% cell lysis at 5:1 E:T ratio across both donors, and 58% versus 61% at an E:T ratio of 20:1. Example 9 – Granulocytic cells of the invention show increased cytocidal activity up to 11-fold over mock transduced granulocytic cells of A549-HER2hi cells when transduced during expansion and with 2 days post-thaw maturation Granulocytic cells of the invention, untransduced granulocytic cells and mock transduced granulocytic cells were thawed into a GREX24 and cultured in IMDM+ 2%HSA+ G-CSF (130ng / ml). The following day A549.Luc2 or A549.Luc2.HER2hi cells were seeded into a white 96 well plate (1E4 / well). Two days post thaw, cultured granulocytic cells of the invention, untransduced granulocytic cells and mock transduced granulocytic cells were counted and resuspended in DMEM10 and seeded onto the target cells at the shown E:T ratios. Lysis was measured after 2 days by the addition of ONEGlo reagent and a comparison of the luminescence from sample wells to target only wells. The results are shown in Figure 9. It was found that with 2 days of maturation, granulocytic cells of the invention showed a modest improvement against A549 compared to UTD or mock granulocytic cells. Using A549-HER2hi cells, markedly higher cytotoxicity was observed with granulocytic cells of the invention comprising a CAR, as compared to mock or untransduced. The comparison of this study with the directly post-thaw assessment shows a marked improvement in the cytocidal activity of the granulocytic cells of the invention against A549- HER2hi cells. The 2 day maturation protocol that improves the cytocidal efficacy of granulocytic cells of the invention replicates conditions that occur on administration of the cells to a subject. Accordingly, it will be noted that it is not just the fact that the cells are expressing higher levels of HER2 that an improvement in cancer killing is observed. The figure shows a fold increase at a 5:1 E:T ratio of at least 7-fold versus the untransduced, and 11-fold versus the mock transduced cells in both the NTP5 and NTP6 donor cells. The Granulocytic cells of the invention also exhibit consistency by means of similar % lysis achieved of both A549 and A549-HER2hi across NTP5 and NTP6 at the E:T ratios of 5:1 and 20:1. The performance of the granulocytic cells of the invention is superior, as would be expected, versus untransduced or mock transduced cells. However, what is unanticipated is the magnitude of the fold increase, in particular at an E:T ratio of 5:1, and it is surprising that a 2 day culture period post-thaw is sufficient to increase the response over granulocytic cells of the invention tested directly post-thaw. Some variability was observed between experiments. For instance, the NTP5 donor untransduced and mock transduced granulocytic cells show unexpectedly high cytocidal activity at an E:T ratio of 20:1, which differs from the majority of the other examples presented. Example 10 – In a human breast cancer cell line (SK-BR3), over 3-fold increases in cytocidal activity were observed in granulocytic cells of the invention over mock transduced and untransduced cells Granulocytic cells of the invention, mock transduced granulocytic cells, and untransduced granulocytic cells were thawed into a GREX24 and cultured in IMDM+ 2%HSA+ G-CSF (130ng / ml). The following day SK-BR—3 cells expressing Luc2 (firefly luciferase) were seeded into a white 96 well plate (1E4 / well).2 days after thawing, cultured granulocytic cells of the invention, mock transduced granulocytic cells, and untransduced granulocytic cells were counted and resuspended in DMEM10 and seeded onto the target cells at the shown E:T ratios. Lysis was measured after 2 days by the addition of ONEGlo reagent and comparison of the luminescence from sample wells to target only wells. The results are shown in Figure 10. Some donor variation was observed with the UTD granulocytic cells, but this was abrogated by the granulocytic cells of the invention performing comparably across both donors. This study shows that the granulocytic cells of the invention have applicability against a different type of cancer cell that also expresses HER2. It was observed that the granulocytic cells of the invention had a cytocidal activity that was consistent across both donors, with an average % lysis of 18% for donor NTP5 cells vs 17% for donor NTP6 cells at 5:1 E:T ratio, and 65% and 63% lysis respectively at an E:T ratio of 20:1. There was some variability in the performance of the untransduced and mock transduced cells across both donors at an E:T ratio of 20:1. Example 11 – Granulocytic cells of the invention show consistent improvements over untransduced and mock transduced cells in alternative methods of culture and with a different donor CD34+ cells of donor NTP015 were thawed and cultured in IMDM 1%HSA, 1% ITS, SCF, FLTL3, TPO (expansion media). After 4h the cells were transduced with viral vectors encoding two different promoters (PGK, miR223) alongside the HER2 CAR.CD3z transgene promoters. The following day the cells were transferred into GREX with more expansion media and the pyrimido-(4,5-b)-indole derivative, UM171. On E4 and E6, the cells were fed with media (of the formulation described above). On E8, the majority of the media was aspirated and differentiation media (Stemline II + SCF, TPO, G-CSF) was added. On E8D2 more differentiation media was added (Stemline II + SCF, TPO, G-CSF, IL-3, GM-CSF). The following day TNFa was added to the cells. The cells were harvested at E8D4 and cryopreserved. Granulocytic cells of the invention, mock transduced granulocytic cells, and untransduced granulocytic cells were thawed into a GREX24 and cultured in IMDM+ 2%HSA+ G-CSF (130ng / ml). The following day A549.Luc2.HER2hi cells were seeded into a white 96 well plate (1E4 / well).2 days after thawing, cultured granulocytic cells of the invention, mock transduced granulocytic cells, and untransduced granulocytic cells were counted and resuspended in DMEM10 and seeded onto the target cells at a 20:1 ratio. Lysis was measured after 2 days by the addition of ONEGlo reagent and by comparing the luminescence from sample wells to target only wells. The results are shown in Figure 11. In this example, the cytocidal activity of the granulocytic cells of the invention was higher directly post-thaw, but 2 days post-thaw remained at least 2-fold higher over the untransduced and 5-fold higher than the mock transduced cells, despite the reduction. A further donor was used and a different culture method; this study therefore shows applicability of the granulocytic cells of the invention to alternative conditions and with different promoters. Example 12 – Granulocytic cells of the invention have a substantially higher cytocidal activity in comparison to neutrophils derived from a cancer patient. Granulocytic cells of the invention, mock transduced granulocytic cells and untransduced granulocytic cells were thawed into a GREX24 and cultured in IMDM+ 2%HSA+ G-CSF (130ng / ml). A549-HER2hi cells were seeded into a white 96 well plate (1E4 / well). The following day after thawing, cultured granulocytic cells of the invention, mock transduced granulocytic cells and untransduced granulocytic cells were counted and resuspended in DMEM10 and seeded onto the target cells at an E:T ratio of 20:1. Alongside this neutrophils were isolated from a cancer patient using a whole blood neutrophil isolation kit (Miltenyi). Lysis was measured after 2 days by the addition of ONEGlo reagent and comparing the luminescence from sample wells to target only wells. Results are shown in Figure 12. Substantially higher killing was elicited by granulocytic cells of the invention compared to neutrophils derived from a cancer patient, an increase of approximately 15-fold. Example 13 – Identification of advantageous methods for modifying cells to express a CAR The inventors undertook the following study to identify advantageous methods by which viral vectors may be used in methods of the invention to modify cells to express CARs. Study design Four sets of experimental transduction protocols were tested for their use to modify cells to express CARs in methods of the invention. As follows, these were viral transduction with nucleic acid encoding a CAR in the presence of: 1. Lentiboost® (a combination of Poloxamer F108 and polybrene), 2. Retronectin with unbound viral vector retained (“RN-keep”), 3. Retronectin with unbound vector removed (“RN-remove”), and 4. Vectofusin. Each transduction protocol was tested at five different multiplicities of infection: 10, 30, 100, 300, 1000. Effectiveness was assessed with respect to proportion of CAR+ cells produced, and intensity of expression of CARs by the cells. Protocol Granulocyte precursor cells were prepared using the v0.4 protocol described elsewhere in this specification. Transduction protocols were performed as follows: Day 0 Retronectin Wells of a non-TC coated plate were coated with 100ul of coating retronectin (diluted in PBS), 20ug / ml The plate was sealed with parafilm and coated left overnight in the fridge CD34 cells were thawed into IMDM – 1% HSA. The cells were CD34 culturecentrifuged and resuspended in 20ml of the expansion media (table on right) Day 1 Virus pre- loading (TD1) pLV[Exp]-CMV>{CD8sp.4D5.CD8tm.CD3z) were thawed at 4C The retronectin from the plate was removed and washed 1x with 100ul of PBS viral vector was added to each well of retronectin coated well as determined by the MOI, with the remained of the being HBSS (final volume 50ul) The plate was centrifuged (2000xg, 32C, 2h) Transduction The cells were resuspended and transferred to a 15ml tube and (TD1) counted. The cell were centrifuged and media was removed to generate cells at 1e6 / ml Vector was removed from one well / retronectin concentration whilst the other well, the vector was kept in the well (Keep and remove conditions) 100ul of cells were added to each virus coated wellsVectofusin stock was diluted 1 / 25 (working solution)For each well 50ul of viral vector (virus + HBSS as determined by MOI) was was mixed with 50ul of vectofusin working solution and incubated for 10min 100ul of cells were added to each well of VF transductionsLentiboost was thawed and added to the wells at the relevant concentration Where necessary the spent media was added to keep the volume / well at 200uL. The plate was sealed with parafilm and centrifuged (400 g, 32C, 45min) The plate was then kept overnight in the incubatorDay 2 transfer to 24wp Cells were transferred to a 24 plate and made up to 2ml with the expansion media Samples of cells were taken for flow cytometry and select Day 6 Flow cytometry conditions were cultured were centrifuged, all the media was aspirate and cultured in IMDM, 1% HSA, 1x ITS and 100ng / ml G- CSF Day 10 Flow Cytometry Cells were counted and taken for flow cytometry- the remaining cells were cryopreserved. Results and conclusions The results of this study are set out in Figure 14 and Figure 15. Figure 14 compares proportion of cells expressing CARs and intensity of CAR expression at different MOIs of viral vector for the different experimental transduction protocols used in the study. Figure 15 compares proportion of cells expressing CARs and intensity of CAR expression over time, in respect of the different experimental transduction protocols used. In both cases, intensity of CAR expression is assessed with reference to mean fluorescence intensity (MFI) of fluorescently labelled CARs. As can be seen transduction using Lentiboost® (a combination of Poloxamer F108 and polybrene) demonstrated marked and surprising advantages as compared to each of the other transduction processes used. With regards to the proportion of CAR+ cells produced, Lentiboost® was the most effective at each MOI tested. Indeed, Lentiboost® at MOI of 30 (or above) achieved a greater proportion of CAR+ cells than any of the other protocols at the same or higher MOIs (even when compared to the alternative protocols at 10-fold or 30+fold higher MOIs, i.e.300 or 1000). This surprising and beneficial increase in effectiveness in terms of the proportion of CAR+ granulocyte precursor cells produced offers previously unexpected advantages in respect of methods of the invention in which combination of Poloxamer F108 and polybrene (such as Lentiboost®) is used to modify cells by viral transduction to express a CAR. This effect was even more pronounced with regards to intensity of CAR expression. Here, the effectiveness of Lentiboost® in terms of intensity of CAR expression rose with increasing MOI from 10 to 300, before plateauing. Transduction using Lentiboost® at MOI of 10 achieved CAR expression intensity greater than that of any of the other test protocols at up to 100-fold higher MOIs. Again, this dramatically increased effectiveness in terms of intensity of CAR expression could not have been predicted, but provides notable and unexpected advantages in respect of methods of the invention in which combination of Poloxamer F108 and polybrene (such as Lentiboost®) is used to modify cells by viral transduction to express a CAR. The benefits noted above were observed at both E6 and E6D4. Lentiboost® at MOI of 30 produced a greater proportion of CAR+ cells and greater intensity of CAR expression than Vectofusin at 100 MOI (3-fold increased MOI) or Retronectin at 1000 MOI (30+ fold increased MOI). The ability to achieve an effective proportion of CAR+ cells and an effective intensity of CAR expression at lower MOIs is preferred due to at least lower cost of using smaller quantities of vector. Example 14: Bulk RNA-sequencing analysis Granulocyte precursor cells produced by the “v0.4” method (a method that may be employed in accordance with the thirteenth aspect of the invention) were used for the following study. Material and methods: Bulk RNA-sequencing was performed by Azenta Life Sciences (Genewiz) using their proprietary method. Briefly, frozen IMAN cell pellets (n=3) were submitted for poly(A)-selected, stranded mRNA library preparation. Libraries were sequenced on an Illumina platform to a depth of ~30 million paired-end reads per sample. Azenta’s “Standard Analysis” pipeline was used, including adapter trimming, alignment to the human reference genome (GRCh38), and quantification at the gene level. Normalized expression was reported as TPM (Transcripts Per Million). TPM measures gene activity in RNA sequencing experiments by counting how many copies of a gene’s RNA there are compared to all the other genes in the same sample, scaled to one million total transcripts. This method further takes into account both the length of each gene and the total amount of RNA sequenced, allowing to compare gene activity within the sample. TPM values were used to determine whether a given gene was very highly, highly, moderately, or lowly expressed or undetectable by comparing the relative abundance of its transcripts within the sample. Specifically, genes associated with: • TPM values <1 TPM were considered to have very low / near-background expression level (or undetectable levels). • TPM values between 1–10 TPM were considered to have low expression levels. • TPM values between 10–100 TPM were considered to have low to moderate expression levels. • TPM values between 100–1000 TPM were considered to have high expression levels. • TPM values >1000 TPM were considered to have very high expression levels. For example, a TPM of 1000 means that out of one million RNA molecules, 1000 come from that gene, while a TPM of 1 means 1 come from that gene (so very low copies). Results: The results of the bulk RNA sequencing analysis are shown in Table 2 below. Specifically, it was found that IMANs of the invention exhibit a unique gene expression profile that is not observed in granulocyte precursors cells of the same developmental stage, which has been differentiated in vivo (wild type cell) or which has been differentiated in vitro using a different method. Specifically, it was observed that IMANs had an increased expression of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) and a decreased expression 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 or differentiated in vitro using a different method. The expression levels for SRGN, MPO, HLA-DRA, CD74, and ELANE were all above 1000 TMP or close to 1000 TPM (very highly expressed), which indicate a particularly high level of expression for these genes. This is surprising because the expression levels for SRGN, MPO, HLA-DRA, CD74, and ELANE were much higher than what is typically observed in natural cells of a comparable developmental stage (e.g. wild type cells from human blood) that has been differentiated in vivo or a cell of a comparable developmental stage that has been differentiated in vitro from a different method. The expression levels of DEFA1, DEFA3, CAMP, BPI, and AZU1 were all below 100 TMP and some below 50 (low to moderate expression), which indicate a particularly low level of expression for these genes. This is surprising because the expression levels for DEFA1, DEFA3, CAMP, BPI, and AZU1 were much lower than what is typically observed in natural cells of a comparable developmental stage (e.g. wild type cells from human blood) that has been differentiated in vivo or a cell of a comparable developmental stage that has been differentiated in vitro from a different method. Thus, the results show that this gene expression profile is not naturally occurring in natural cells (wild type cells in an organism or a subject – in vivo differentiated) demonstrating that the methods of the invention lead to the production of granulocytes precursors endowed with characteristics and advantages as described above, which are not observed in nature nor in any granulocyte precursors cells of the same developmental stage that have been differentiated in vitro from a different method. Table 2: Gene expression profile Genes NCBI Gene ID Ensembl_Gene_ID TPM (Mean Numbers expression N=3) Serglycin (SRGN) 5552 ENSG00000122862 7939 Myeloperoxidase (MPO) 4353 ENSG00000005381 5515 MHC class II, DR alpha 3122 ENSG00000204287 2202 (HLA-DRA) CD74 (CD74) 972 ENSG00000019582 1671 Neutrophil Elastase 1991 ENSG00000197561 1659 (ELANE) Defensin alpha 1 1667 ENSG00000206047 0 (DEFA1) Defensin alpha 3 1668 ENSG00000239839 32 (DEFA3) Cathelicidin antimicrobial 820 ENSG00000164047 1.6 peptide (CAMP) Bactericidal / Permeability- 671 ENSG00000101425 194 Increasing Protein (BPI) Azurocidin 1 (AZU1) 566 ENSG00000172232 936 NCBI Gene ID numbers are available at: https: / / www.ncbi.nlm.nih.gov / gene (last updated 19 September 2025). Ensembl_Gene_ID numbers are available at: https: / / www.ensembl.org (last updated 19 September 2025). Example 15A: Selection of donors Donors providing cells to be used in the preparation of cells of the invention, and cell populations of the invention, used in the preceding Examples 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 15B 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 15B); and b. fulfilled the selection criteria in Tables A, B and C: Table A: Inclusion criteria: 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 15B: 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 16A and 16B. 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 16C), 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 SupT1 SupT1 Staurosporine Staurosporine (n=3) [20:1] [40:1] [0.2 µM] [10 µM] [40:1] % Lysis 70 65 85 30 95 SPECIFIC ASPECTS AND EMBODIMENTS OF THE INVENTION The following paragraphs do not constitute claims, but do set out certain subject matter, including aspects and embodiment of the invention, in respect of which protection may be sought and priority claimed. 1. A population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) 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 • less than 50% of the cells of the population express HLA-DR. 2. A population according to paragraph 1, wherein approximately 55 to 65% of the cells of the population express CD11b. 3. A population according to paragraph 1 or paragraph 2, wherein approximately 70 to 90% of the cells of the population express CD15. A population according to any of paragraphs 1 to 3, wherein approximately 70 to 90% of the cells of the population express CD64. A population according to any of paragraphs 1 to 4, wherein approximately 75 to 95% of the cells of the population express CD89. A population according to any of paragraphs 1 to 5, wherein approximately 50 to 70% of the cells of the population express CXCR2. A population according to any of paragraphs 1 to 6, wherein approximately 60 to 80% of the cells of the population express neutrophil elastase. A population according to any of paragraphs 1 to 7, wherein approximately 0 to 10% of the cells of the population express CD14. A population according to any of paragraphs 1 to 8, wherein approximately 0 to 2.5% of the cells of the population express CD19. A population according to any of paragraphs 1 to 9, wherein approximately 0 to 2.5% of the cells of the population express CD3. A population according to any of paragraphs 1 to 10, wherein approximately 0 to 10% of the cells of the population express CD34. A population according to any of paragraphs 1 to 11, wherein approximately 0 to 20% of the cells of the population express CD66b. A population according to any of paragraphs 1 to 12, wherein approximately 0 to 2.5% of the cells of the population express CD68. A population according to any of paragraphs 1 to 13, wherein approximately 20 to 40% of the cells of the population express CXCR4. A population according to any of paragraphs 1 to 14, wherein approximately 20 to 40% of the cells of the population express HLA-DR. 16. A population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) wherein: • a first subpopulation of cells are CD15+ CD64+ CD18+ CD49d+ CD71+; • a second subpopulation of cells are CD15- CD11b+ / - CD18+ CD49d+ CD32+ HLA- DR-; and • a third subpopulation of cells are CD15- CD11b- HLA-DR+ CD18+ CD49d+ and CD71+. 17. A population according to any of the preceding paragraphs, having cytocidal activity that is increased by at least 2.5-fold as compared to a control cell population. 18. A population according to paragraph 17, wherein the cytocidal activity is increased by at least 4-fold as compared to a control cell population. 19. A population according to paragraph 18 wherein the cytocidal activity is increased by at least 8-fold as compared to a control cell population. 20. A population according to paragraph 19, wherein the cytocidal activity is increased by at least 15-fold as compared to a control cell population. 21. A population according to any of paragraphs 17 to 20, wherein the control cell population is selected from the group consisting of: a population of granulocytes or precursors thereof having the marker profile recited in paragraph 1 or in paragraph 16, that do not comprise a CAR; and a population of unmodified granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) from a subject. 22. A population according to paragraph 21, wherein the subject is selected from the group consisting of: a healthy subject, and a cancer patient subject. 23. A population according to any of paragraphs 17 to 22, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of at least 20:1. 24. A population according to any of paragraphs 17 to 22, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of at least 5:1. A population according to paragraph 24, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of 5:1. A population according to any of paragraphs 1 to 25, comprising a CAR specific for an antigen selected from the group consisting of: a tumour associated antigen (TAA); a pathogen associated antigen; and an autoimmune disease associated antigen. A population according to paragraph 26, wherein the CAR is specific for a TAA associated with solid tumours. A pharmaceutical composition comprising a population according to any of paragraphs 1 to 27. A population according to any of paragraphs 1 to 27, or a pharmaceutical composition according to paragraph 28, for use as a medicament. A population or pharmaceutical composition for use according to paragraph 29, in the treatment of cancer. A population or pharmaceutical composition for use according to paragraph 30, wherein the CAR is specific for a TAA. A population or pharmaceutical composition for use according to paragraph 29, wherein the TAA is 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. A population or pharmaceutical composition for use according to paragraph 29, in the treatment of an infectious disease. A population or pharmaceutical composition for use according to paragraph 33, wherein the CAR is specific for a pathogen associated antigen. A population or pharmaceutical composition for use according to paragraph 29, in the treatment of an autoimmune disease. A population or pharmaceutical composition for use according to paragraph 35, wherein the CAR is specific for an autoimmune disease associated antigen. A population or pharmaceutical composition for use according to any of paragraphs 29 to 36, wherein treatment comprises cytocidal activity of the granulocytes or precursors thereof in respect of cells expressing the antigen for which the CAR is specific. A population or pharmaceutical composition for use according to paragraph 37, wherein treatment is by means of cytocidal activity of the granulocytes or precursors thereof in respect of cells expressing the antigen for which the CAR is specific. A population or pharmaceutical composition for use according to any of paragraphs 29 to 38, wherein treatment comprises therapeutic immunomodulatory activity by the granulocytes or precursors thereof. A method of preparing cells for therapeutic use, the method comprising culturing stem or progenitor cells in cell culture conditions that induce the formation of a population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) having the marker profile rec paragraph 1, wherein the method comprises modifying the cells to express a CAR. A method according to paragraph 40, wherein the modification of the cells to express a CAR comprises a transduction step utilising a nucleic acid encoding the CAR. A method according to paragraph 40 or paragraph 41, wherein the method comprises a differentiation step promoting differentiation of progenitor cells to the granulocytes or precursors thereof, the differentiation step comprising cell culture conditions comprising the presence of: • G-CSF, • GM-CSF, • IL-3, • and TNF. A method according to paragraph 42, wherein the differentiation step further comprises cell culture condition comprising at least one supplement from the group consisting of: SCF, TPO, ITS, and HSA. A method according to paragraph 42 or paragraph 43, wherein the method comprises a differentiation step promoting differentiation of progenitor cells to the granulocytes or precursors thereof, the differentiation step comprising cell culture conditions comprising the presence of: • SCF, • TPO, and • G-CSF. A method according to paragraph 44, wherein the differentiation step further comprises cell culture conditions comprising at least one supplement from the group consisting of: • GM-CSF, • IL-3, • TNF. A method according to any of paragraphs 43 to 45, wherein the SCF, TPO, and G-CSF are provided in an amount determined based upon the number of cells in culture. A method according to paragraph 46 wherein the amount is approximately 0.333 ng per 1000 cells in a first incidence of treatment, and approximately 0.666 ng per 1000 cells in a second incidence of treatment. A method according to any of paragraphs 42 to 47, wherein the cell culture conditions comprise an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, Flt-3 ligand, IL-3, IL- 6, and TPO. A method according to any of paragraphs 42 to 48, wherein the cell culture conditions comprise an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells. A method according to paragraph 49, wherein the pyrimido-[4,5-b]-indole derivative is selected from the group consisting of: UM171, and UM729. A method according to paragraph 50, wherein the pyrimido-[4,5-b]-indole derivative is UM171. A method according to paragraph 50 or paragraph 51, wherein the expansion step further comprises the presence of IL-3 and / or IL-6. A method according to any of paragraphs 49 to 52, wherein the expansion step further comprises the presence of ITS and / or HAS. A method according to any of paragraphs 42 to 53, wherein a differentiation step according to any of paragraphs 39 to 44, is preceded by an expansion step according to any of paragraphs 48 to 53. A method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, Flt-3 ligand, IL-3, IL-6, and TPO; and modifying the cells to express a CAR. A method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells; and modifying the cells to express a CAR. A method according to paragraph 55 or paragraph 56, wherein the modification of the cells to express a CAR comprises a transduction step utilising a nucleic acid encoding the CAR. A method according to paragraph 56 or paragraph 57, wherein the pyrimido-[4,5-b]- indole derivative is selected from the list consisting of: UM171; and UM729. A method according to paragraph 58 wherein the pyrimido-[4,5-b]-indole derivative is UM171. A method according to any of paragraphs 55 to 59, wherein the expansion step further comprises the presence of IL-3 and IL-6. A method according to any of paragraphs 55 to 60, wherein the expansion step further comprises the presence of ITS and / or HAS. A method of preparing cells for therapeutic use, the method comprising culturing progenitor cells in cell culture conditions comprising a differentiation step, comprising the presence of G-CSF, GM-CSF, IL-3, and TNF; and modifying the cells to express a CAR. A method according to paragraph 62, wherein the differentiation step further comprises at least one supplement from the group consisting of: SCF, TPO, ITS, and HSA. A method of preparing cells for therapeutic use, the method comprising culturing progenitor cells in cell culture conditions comprising a differentiation step, comprising the presence of SCF, TPO, G-CSF, GM-CSF, IL-3, and TNF; and a transduction step utilising a nucleic acid encoding a CAR. A method according to paragraph 64, wherein the SCF, TPO, and G-CSF are provided in an amount determined based upon the number of cells in culture. A method according to paragraph 64, wherein the amount is approximately 0.333 ng per 1000 cells in a first incidence of treatment, and approximately 0.666 ng per 1000 cells in a second incidence of treatment. A method according to any of paragraphs 42 to 66, wherein the modification of the cells to express a CAR is applied prior to the differentiation step. A method according to any of paragraphs 42 to 66, wherein the modification of the cells to express a CAR is applied during the differentiation step. A method according to any of paragraphs 47 to 68, wherein the modification of the cells to express a CAR is applied prior to the expansion step. A method according to any of paragraphs 47 to 68, wherein the modification of the cells to express a CAR is applied during the expansion step. A method according to any of paragraphs 47 to 68, wherein the modification of the cells to express a CAR is applied after the expansion step. A method according to paragraph 67 or paragraph 71, wherein the modification of the cells to express a CAR is applied between the differentiation step and the expansion step. A method according to any of the preceding paragraphs, wherein modification of the cells to express a CAR comprises transduction of the cells with a nucleic acid encoding the CAR. A method according to paragraph 73, wherein the transduction is carried out by means of a viral vector. A method according to paragraph 73 or paragraph 74, wherein the cells are transduced on the first day of the expansion step. A method according to any of paragraph 40 to 75, wherein the CAR is specific for an antigen selected from the group consisting of: a TAA; a pathogen associated antigen; and an autoimmune disease associated antigen. A method according to any one of paragraphs 40 to 76, wherein at least 5% of the granulocytes or precursors thereof express a CAR. A method according to paragraph 77, wherein at least 25% of the granulocytes or precursors thereof express a CAR. A method according to paragraph 78, wherein at least 50% of the granulocytes or precursors thereof express a CAR. A. A population of granulocytes, or precursors thereof, comprising granulocytes, or precursors thereof, expressing a chimeric antigen receptor (CAR) 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 • less than 50% of the cells of the population express HLA-DR. B. A population according to paragraph A, wherein approximately 55 to 65% of the cells of the population express CD11b. C. A population according to paragraph A or paragraph B, wherein approximately 70 to 90% of the cells of the population express CD15. D. A population according to any of paragraphs A to C, wherein approximately 70 to 90% of the cells of the population express CD64. E. A population according to any of paragraphs A to D, wherein approximately 75 to 95% of the cells of the population express CD89. F. A population according to any of paragraphs A to E, wherein approximately 50 to 70% of the cells of the population express CXCR2. G. A population according to any paragraphs A to F, wherein approximately 60 to 80% of the cells of the population express neutrophil elastase. H. A population according to any of paragraphs A to G, wherein approximately 0 to 10% of the cells of the population express CD14. I. A population according to any of paragraphs A to H, wherein approximately 0 to 2.5% of the cells of the population express CD19. J. A population according to any of paragraphs A to I, wherein approximately 0 to 2.5% of the cells of the population express CD3. K. A population according to any of paragraphs A to J, wherein approximately 0 to 10% of the cells of the population express CD34. L. A population according to any of paragraphs A to K, wherein approximately 0 to 20% of the cells of the population express CD66b. M. A population according to any of paragraphs A to L, wherein approximately 0 to 2.5% of the cells of the population express CD68. N. A population according to any of paragraphs A to M, wherein approximately 20 to 40% of the cells of the population express CXCR4. O. A population according to any of paragraphs A to N, wherein approximately 20 to 40% of the cells of the population express HLA-DR. P. A population of granulocytes, or precursors thereof, comprising granulocytes, or precursors thereof, expressing a chimeric antigen receptor (CAR) wherein: • a first subpopulation of cells are CD15+ CD64+ CD18+ CD49d+ CD71+; • a second subpopulation of cells are CD15- CD11b+ / - CD18+ CD49d+ CD32+ HLA- DR-; and • a third subpopulation of cells are CD15- CD11b- HLA-DR+ CD18+ CD49d+ and CD71+. Q. A population according to any of paragraphs A to P, wherein the cytocidal activity is increased by at least 4-fold as compared to a control cell population. R. A population according to paragraph Q, wherein the cytocidal activity is increased by at least 15-fold as compared to a control cell population. S. A population according to paragraph Q or paragraph R, wherein the control cell population is selected from the group consisting of: a population of granulocytes or precursors thereof having the marker profile recited in claim 1 or in claim 16, that do not comprise a CAR; and a population of unmodified granulocytes, or precursors thereof, from a subject. T. A population according to any of paragraphs Q to S, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of at least 5:1. U. A population according to any of paragraphs A to T, comprising a CAR specific for an antigen selected from the group consisting of: a tumour associated antigen (TAA); a pathogen associated antigen; and an autoimmune disease associated antigen. V. A pharmaceutical composition comprising a population according to any of paragraphs A to U. W. A population according to any of paragraphs A to U, or a pharmaceutical composition according to claim 22, for use as a medicament. X. A population or pharmaceutical composition for use according to paragraph W, in the treatment of cancer. Y. A population or pharmaceutical composition for use according to paragraph X, wherein the CAR is 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.

Claims

CLAIMS 1. A granulocyte precursor cell comprising a chimeric antigen receptor (CAR).

2. A granulocyte precursor cell according to claim 1, comprising: • 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 • 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.

3. A population of granulocyte precursor cells, comprising or consisting of granulocyte precursor cells according to claim 2.

4. A population of granulocyte precursor cells, the population comprising one or more granulocyte precursor cells expressing a CAR.

5. A population according to claim 4, comprising a granulocyte precursor cell according to claim 2.

6. A population of granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) comprising granulocytes, or precursors thereof, (e.g., granulocyte precursor cells) expressing a chimeric antigen receptor (CAR) 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 • less than 50% of the cells of the population express HLA-DR.

7. A population according to claim 6, wherein approximately 55 to 65% of the cells of the population express CD11b.

8. A population according to any of claims 3 to 7, wherein approximately 70 to 90% of the cells of the population express CD15.

9. A population according to any of claims 3 to 8, wherein approximately 70 to 90% of the cells of the population express CD64.

10. A population according to any of claims 3 to 9, wherein approximately 75 to 95% of the cells of the population express CD89.

11. A population according to any of claims 3 to 10, wherein approximately 50 to 70% of the cells of the population express CXCR2.

12. A population according to any of claims 1 to 11, wherein approximately 60 to 80% of the cells of the population express neutrophil elastase.

13. A population according to any of claims 3 to 12, wherein approximately 0 to 10% of the cells of the population express CD14.

14. A population according to any of claims 3 to 13 wherein approximately 0 to 2.5% of the cells of the population express CD19.

15. A population according to any of claims 3 to 14, wherein approximately 0 to 2.5% of the cells of the population express CD3.

16. A population according to any of claims 3 to 15, wherein approximately 0 to 10% of the cells of the population express CD34.

17. A population according to any of claims 3 to 16, wherein approximately 0 to 20% of the cells of the population express CD66b.

18. A population according to any of claims 3 to 17, wherein approximately 0 to 2.5% of the cells of the population express CD68.

19. A population according to any of claims 3 to 18, wherein approximately 20 to 40% of the cells of the population express CXCR4.

20. A population according to any of claims 3 to 19, wherein approximately 20 to 40% of the cells of the population express HLA-DR.

21. A population of granulocyte precursor cells comprising granulocyte precursor cells expressing a chimeric antigen receptor (CAR) wherein: • a first subpopulation of cells is CD15+ CD64+ CD18+ CD49d+ CD71+; • a second subpopulation of cells is CD15- CD11b+ / - CD18+ CD49d+ CD32+ HLA-DR- ; and • a third subpopulation of cells is CD15- CD11b- HLA-DR+ CD18+ CD49d+ and CD71+.

22. A granulocyte precursor cell, or cell population, according to any of the preceding claims, having cytocidal activity that is increased by at least 2.5-fold as compared to a control cell or cell population.

23. A granulocyte precursor cell, or cell population, according to claim 22, wherein the cytocidal activity is increased by at least 4-fold as compared to a control cell or cell population.

24. A granulocyte precursor cell, or cell population, according to claim 23 wherein the cytocidal activity is increased by at least 8-fold as compared to a control cell or cell population.

25. A granulocyte precursor cell, or cell population, according to claim 24, wherein the cytocidal activity is increased by at least 15-fold as compared to a control cell or cell population.

26. A granulocyte precursor cell, or cell population, according to any of claims 22 to 25, wherein the control cell or cell population is selected from the group consisting of: a population of granulocytes precursor cells having the marker profile recited in claim 2, claim 5, or in claim 20, that do not comprise a CAR; and an unmodified granulocyte precursor cell, or population of unmodified granulocyte precursor cells, from a subject.

27. A granulocyte precursor cell, or cell population, according to claim 26, wherein the subject is selected from the group consisting of: a healthy subject, and a cancer patient subject.

28. A granulocyte precursor cell, or cell population, according to any of claims 22 to 27, wherein cytocidal activity is assessed at an effector:target cell ratio of at least 20:

1.

29. A granulocyte precursor cell, or cell population, according to any of claims 22 to 27, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of at least 5:

1.

30. A granulocyte precursor cell, or cell population, according to claim 29, wherein cytocidal activity of the cells is assessed at an effector:target cell ratio of 5:

1. 31 A granulocyte precursor cell, or cell population, according to any of claims 1 to 30, comprising a CAR specific for an antigen selected from the group consisting of: a tumour associated antigen (TAA); a pathogen associated antigen; and an autoimmune disease associated antigen.

32. A granulocyte precursor cell, or cell population, according to claim 30, wherein the CAR is specific for a TAA associated with solid tumours.

33. A granulocyte precursor cell, or cell population, according to any preceding claim, wherein the granulocyte precursor cell, or cell population, has been derived from a donor having a granulocyte (neutrophil) with high CKA.

34. A granulocyte, or granulocyte precursor (preferably a granulocyte precursor cell) expressing a CAR.

35. A pharmaceutical composition comprising a granulocyte precursor cell, or cell population, according to any of claims 1 to 34.

36. A granulocyte precursor cell, or cell population, according to any of claims 1 to 34, or a pharmaceutical composition according to claim 35, for use as a medicament.

37. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 36, in the treatment of cancer.

38. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 37, treatment of one or more of: cervical cancer (such as metastatic cervical cancer), head and neck cancer, pancreatic cancer, liver cancer, oesophageal cancer, stomach 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.

39. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 37 or claim 38, wherein the CAR is specific for a TAA.

40. A population or pharmaceutical composition for use according to claim 39, wherein the TAA is 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.

41. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 36, in the treatment of an infectious disease.

42. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 41, wherein the CAR is specific for a pathogen associated antigen.

43. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 36, in the treatment of an autoimmune disease.

44. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 43, wherein the CAR is specific for an autoimmune disease associated antigen.

45. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to any of claims 36 to 44, wherein treatment comprises cytocidal activity of the granulocytes or precursors thereof in respect of cells expressing the antigen for which the CAR is specific.

46. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to claim 41, wherein treatment is by means of cytocidal activity of the granulocytes or precursors thereof in respect of cells expressing the antigen for which the CAR is specific.

47. A granulocyte precursor cell, or cell population, or pharmaceutical composition for use according to any of claims 36 to 46, wherein treatment comprises therapeutic immunomodulatory activity by the granulocytes or precursors thereof.

48. Use of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim, in the manufacture of a medicament for treating cancer.

49. Use of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim, in the manufacture of a medicament for treating an infection.

50. Use of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim, in the manufacture of a medicament for treating an autoimmune disease.

51. A method for treating cancer, the method comprising administering to a subject in need thereof a therapeutically effective amount of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim.

52. A method for treating an infection, the method comprising administering to a subject in need thereof a therapeutically effective amount of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim.

53. A method for treating an autoimmune disease, the method comprising administering to a subject in need thereof a therapeutically effective amount of a granulocyte precursor cell, or cell population, or pharmaceutical composition according to any preceding claim.

54. A method of preparing cells for therapeutic use, the method comprising culturing stem or progenitor cells in cell culture conditions that induce the formation of a population of granulocyte precursor cells having markers as defined in claim 2 or in any of claims 6 to 21, wherein the method comprises modifying the cells to express a CAR.

55. A method according to claim 54, wherein the modification of the cells to express a CAR comprises a transduction step utilising a nucleic acid encoding the CAR.

56. A method according to claim 54 or claim 55, wherein the method comprises a differentiation step promoting differentiation of progenitor cells to the granulocytes or precursors thereof, the differentiation step comprising cell culture conditions comprising the presence of: • G-CSF, • GM-CSF, • IL-3, • and TNF.

57. A method according to claim 56, wherein the differentiation step further comprises cell culture condition comprising at least one supplement from the group consisting of: SCF, TPO, ITS, and HSA.

58. A method according to claim 56 or claim 57, wherein the method comprises a differentiation step promoting differentiation of progenitor cells to the granulocytes or precursors thereof, the differentiation step comprising cell culture conditions comprising the presence of: • SCF, • TPO, and • G-CSF.

59. A method according to claim 58, wherein the differentiation step further comprises cell culture conditions comprising at least one supplement from the group consisting of: • GM-CSF, • IL-3, • TNF.

60. A method according to claim 58 or claim 59, wherein the SCF, TPO, and G-CSF are provided in an amount determined based upon the number of cells in culture.

61. A method according to claim 60 wherein the amount is approximately 0.333 ng per 1000 cells in a first incidence of treatment, and approximately 0.666 ng per 1000 cells in a second incidence of treatment.

62. A method according to any of claims 56 to 61, wherein the cell culture conditions comprise an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, Flt-3 ligand, IL-3, IL- 6, and TPO.

63. A method according to any of claims 56 to 62, wherein the cell culture conditions comprise an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells.

64. A method according to claim 63, wherein the pyrimido-[4,5-b]-indole derivative is selected from the group consisting of: UM171, and UM729.

65. A method according to claim 64, wherein the pyrimido-[4,5-b]-indole derivative is UM171.

66. A method according to claim 64 or claim 65, wherein the expansion step further comprises the presence of IL-3 and / or IL-6.

67. A method according to any of claims 63 to 66, wherein the expansion step further comprises the presence of ITS and / or HAS.

68. A method according to any of claims 56 to 67, wherein a differentiation step according to any of claims 43 to 48, is preceded by an expansion step according to any of claims 52 to 57.

69. A method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, Flt-3 ligand, IL-3, IL-6, and TPO; and modifying the cells to express a CAR.

70. A method of preparing cells for therapeutic use, the method comprising culturing stem cells in cell culture conditions comprising an expansion step promoting expansion of cell number and formation of progenitor cells from stem cells, comprising the presence of SCF, FLT3-L, TPO, and a pyrimido-[4,5-b]-indole derivative that promotes the expansion of hematopoietic stem cells; and modifying the cells to express a CAR.

71. A method according to claim 69 or claim 70, wherein the modification of the cells to express a CAR comprises a transduction step utilising a nucleic acid encoding the CAR.

72. A method according to claim 70 or claim 71, wherein the pyrimido-[4,5-b]-indole derivative is selected from the list consisting of: UM171; and UM729.

73. A method according to claim 72 wherein the pyrimido-[4,5-b]-indole derivative is UM171.

74. A method according to any of claims 69 to 73, wherein the expansion step further comprises the presence of IL-3 and IL-6.

75. A method according to any of claims 69 to 74, wherein the expansion step further comprises the presence of ITS and / or HAS.

76. A method of preparing cells for therapeutic use, the method comprising culturing progenitor cells in cell culture conditions comprising a differentiation step, comprising the presence of G-CSF, GM-CSF, IL-3, and TNF; and modifying the cells to express a CAR.

77. A method according to claim 76, wherein the differentiation step further comprises at least one supplement from the group consisting of: SCF, TPO, ITS, and HSA.

78. A method of preparing cells for therapeutic use, the method comprising culturing progenitor cells in cell culture conditions comprising a differentiation step, comprising the presence of SCF, TPO, G-CSF, GM-CSF, IL-3, and TNF; and a transduction step utilising a nucleic acid encoding a CAR.

79. A method according to claim 78, wherein the SCF, TPO, and G-CSF are provided in an amount determined based upon the number of cells in culture.

80. A method according to claim 79, wherein the amount is approximately 0.333 ng per 1000 cells in a first incidence of treatment, and approximately 0.666 ng per 1000 cells in a second incidence of treatment.

81. A method according to any of claims 56 to 80, wherein the modification of the cells to express a CAR is applied prior to the differentiation step.

82. A method according to any of claims 56 to 80, wherein the modification of the cells to express a CAR is applied during the differentiation step.

83. A method according to any of claims 63 to 82, wherein the modification of the cells to express a CAR is applied prior to the expansion step.

84. A method according to any of claims 62 to 82, wherein the modification of the cells to express a CAR is applied during the expansion step.

85. A method according to any of claims 62 to 82, wherein the modification of the cells to express a CAR is applied after the expansion step.

86. A method according to claim 82 or claim 85, wherein the modification of the cells to express a CAR is applied between the differentiation step and the expansion step.

87. A method according to any of claims 54 to 86, wherein modification of the cells to express a CAR comprises transduction of the cells with a nucleic acid encoding the CAR.

88. A method according to claim 87, wherein the transduction is carried out by means of a viral vector.

89. A method according to claim 88, wherein the viral vector is selected from the group consisting of: a CMV vector; an LV vector; an MMLV vector; and a MSCV vector.

90. A method according to claim 89, wherein the viral vector is a CMV viral vector.

91. A method according to any of claims 88 to 90, wherein transduction is performed in the presence of a combination of Poloxamer F108 and polybrene (such as Lentiboost®).

92. A method according to any of claims 88 to 91, wherein transduction is performed using a viral vector at an MOI of between approximately 10 and approximately 1000.

93. A method according to any of claims 87 or claim 92, wherein the cells are transduced on the first day of the expansion step.

94. A method according to any of claim 54 to 93, wherein the CAR is specific for an antigen selected from the group consisting of: a TAA; a pathogen associated antigen; and an autoimmune disease associated antigen.

95. A method according to any one of claims 54 to 94, wherein at least 5% of the granulocytes or precursors thereof express a CAR.

96. A method according to claim 95, wherein at least 25% of the granulocytes or precursors thereof express a CAR.

97. A method according to claim 96, wherein at least 50% of the granulocytes or precursors thereof express a CAR.

98. A method according to claim 97, wherein at least 60% of the granulocytes or precursors thereof express a CAR.

99. A method according to claim 98, wherein at least 70% of the granulocytes or precursors thereof express a CAR.

100. A method according to claim 99, wherein at least 80% of the granulocytes or precursors thereof express a CAR.

101. A method of preparing cells for therapeutic use, as herein described.

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