Improved intratumoral DC therapies

Abstract

The present disclosure relates to compositions and methods of making short-term-matured alpha-type 1-dendritic (ST-αDC1) cells, and the use thereof.

Description

[0001] Attorney Docket No: 11390-018WO1 IMPROVED INTRATUMORAL DC THERAPIES STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH This invention was made with government support under Grant No. P01CA234212 awarded by the National Institutes of Health (NIH). The government has certain rights in the invention. CROSS REFERENCE TO RELATED APPLICATIONS This application claims the benefit of U.S. Provisional Application No.63 / 594,096, filed on October 30, 2023, which is incorporated herein by reference in its entirety. BACKGROUND Dendritic cells (DC) have been shown to be able to induce effective cancer immunity in experimental animals and cancer patients, leading to their applications as cancer therapies. Three groups of factors needed for their clinical activity: a) ability to present antigens (“signal 1”); b) ability to provide costimulatory factors (“signal 2”); c) ability to migrate to the draining lymph nodes and d) ability to produce IL-12 during contact with antigen specific T cells (“signal 3”), are differentially regulated at different stages of DC maturation, and limited by the maturation- associated DC “exhaustion” making it difficult to generate DC product optimized for all these features. What is needed is a strategy to utilize the limited DC maturation period effectively to improve DC cell therapy. SUMMARY Disclosed herein are compositions and methods of making short-term-matured alpha-type 1-dendritic (ST-αDC1) cells, and the use thereof. In one aspect disclosed herein, are methods of making one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (such as for example, 4x4 ST-αDC1), comprising culturing one or more monocytic cell(s) with GM-CSF, IL-4 or a combination thereof, for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to a αDC1 cell maturation cocktail comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C)) for less than 18 hours. In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are formulated in a unitary composition. In some Attorney Docket No: 11390-018WO1 aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are maintained separately. In some aspects, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. Also disclosed herein are methods of making one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (such as for example, 4x4 ST-αDC1) of any preceding aspect, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml and / or the TLR3 ligand (such as for example, Polyinosinic:polycytidylic acid (poly-I:C)) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some aspects, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). In some aspects, the one or more ST- αDC1 cell(s) is loaded with at least one or more antigenic peptides. In some aspects, disclosed herein are methods of making one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (such as for example, 4x4 ST-αDC1) of any preceding aspect, wherein the one or more ST-αDC1 cell(s) produces at least a 50% increased IL-12p70, at least a 50% increased CXCL10, and / or at least a 50% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). Also disclosed herein, are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition (such as, for example, glioma, brain cancer (including, but not limited to recurrent brain cancer), anaplastic astrocytoma (AA), and melanoma (including, but not limited to checkpoint-resistant metastatic melanoma)) in a subject comprising; administering to the subject a therapeutically effective amount of one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (including, but not limited to 4x4 ST-αDC1) made by the method of any of the preceding aspects. For example, disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition (such as, for example, glioma, brain cancer (including, but not limited to recurrent brain cancer), anaplastic astrocytoma (AA), and melanoma (including, but not limited to checkpoint-resistant metastatic melanoma)) in a subject comprising; administering to the subject a therapeutically effective amount of one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (including, but not limited to 4x4 ST-αDC1), wherein the one or more ST-αDC1 cell(s) are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a Attorney Docket No: 11390-018WO1 combination thereof for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C), for less than 18 hours, resulting in the one or more ST-αDC1 cell(s). In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are formulated in a unitary composition. In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are maintained separately. In some aspects, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. In some aspects disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition of any preceding aspect, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml and / or the TLR3 ligand (such as for example, Polyinosinic:polycytidylic acid (poly-I:C)) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some aspects, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). In some aspects, the one or more ST- αDC1 cell(s) is loaded with at least one or more antigenic peptides. Also disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition of any preceding aspect, wherein the one or more ST-αDC1 cell(s) produces at least a 50% increased IL- 12p70, at least a 50% increased CXCL10, and / or at least a 50% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). Also disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition of any preceding aspect, wherein the one or more ST-αDC1 cell(s) increases intratumoral accumulation of cytotoxic T lymphocytes (CTLs) compared to a control and sensitizes tumors to anti-PD1 therapy. In some aspects, the one or more ST-αDC1 cell(s) can be administered to the subject as a systemic injection, intratumorally or within a peritumoral intracavity. In some aspects, the method further comprises isolating one or more T cells from the subject, sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST-αDC1 cell(s) ex vivo, and administering to the subject, the one or more ex vivo-sensitized T cell(s). Attorney Docket No: 11390-018WO1 In one aspect disclosed herein are adoptive cell therapies comprising one or more ST- αDC1 cell(s) and / or one or more in vitro or ex vivo-sensitized T cell(s). In some embodiments, the one or more in vitro or ex vivo-sensitized T cell(s) is activated by one or more ST-αDC1 cell(s), which are made by a method of any preceding aspect. For example, disclosed herein are adoptive cell therapies comprising one or more ST-αDC1 cell(s) and / or one or more in vitro or ex vivo-sensitized T cell(s). In some embodiments, the one or more in vitro or ex vivo-sensitized T cell(s) is activated by one or more ST-αDC1 cell(s), which are made by a method comprising culturing one or more monocytic cell(s) with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail (comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C), for less than 18 hours, resulting in the one or more ST-αDC1 cell(s). In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are formulated in a unitary composition. In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are maintained separately. In some aspects, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. Also disclosed herein are adoptive therapies of any preceding aspect, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml and / or the TLR3 ligand (such as for example, Polyinosinic:polycytidylic acid (poly-I:C)) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some aspects, the one or more ST-αDC1 cell(s) is loaded with at least one or more antigenic peptides. In some aspects, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). In some aspects, disclosed herein are adoptive therapies of any preceding aspect, wherein the in vitro or ex vivo-sensitized T cell has an increase in its Th1, cytotoxic T lymphocyte (CTL) and / or NK-like function, compared to an unsensitized T cell. Also disclosed herein, are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition (such as, for example, glioma, brain cancer (including, but not limited to recurrent brain cancer), anaplastic astrocytoma (AA), and melanoma (including, but not limited to checkpoint-resistant Attorney Docket No: 11390-018WO1 metastatic melanoma)) in a subject comprising a) isolating one or more T cell(s) from the subject, b) sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST-αDC1 cell(s) ex vivo, wherein the one or more ex vivo-sensitized T cell(s); and c) administering to a subject in need thereof, the one or more ex vivo-sensitized T cell(s), wherein the one or more ST-αDC1 cell(s) are made by a method of any preceding aspect, including, but not limited to, culturing one or more monocytic cell(s) with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail (comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and TLR3 ligand (such as for example, Polyinosinic:polycytidylic acid (poly-I:C)), for less than 18 hours, resulting in the one or more ST-αDC1 cell(s). In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are formulated in a unitary composition. In some aspects, the IL1β, TNFα, IFNα, IFNγ, and TLR3 ligand are maintained separately. In some aspects, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. In some aspects, the one or more ST-αDC1 cell(s) is loaded with at least one or more antigenic peptides. In some aspects, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). In some aspects disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition of any preceding aspect, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml and / or the TLR3 ligand (such as for example, Polyinosinic:polycytidylic acid (poly-I:C)) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some aspects, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). In some aspects, the one or more ST- αDC1 cell(s) is loaded with at least one or more antigenic peptides. Also disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition of any preceding aspect, wherein the in vitro or ex vivo-sensitized T cell has an increase in its Th1, cytotoxic T lymphocyte (CTL) and / or NK-like function, compared to an unsensitized T cell. Attorney Docket No: 11390-018WO1 BRIEF DESCRIPTION OF THE DRAWINGS The accompanying drawings, which are incorporated in and constitute a part of this specification, illustrate several embodiments and together with the description illustrate the disclosed compositions and methods. Figure 1 shows the clinical activity of αDC1 vaccines in patients with brain cancer and PD1-non-responsive metastatic melanoma. Left panel shows complete radiologic response to vaccination with αDC1s loaded glioma stem-cells-targeting antigenic peptides in a patient with recurrent glioma (MRI). Objective responses (all long-lasting) were observed in a total of 4 / 19 patients (3 more patients after publication of our 2011 paper). Middle panel shows correlation between IL-12p70 production by αDC1 vaccines of the individual patients (in vitro; after 24h CD40L stimulation; ELISA) and the patients’ progression-free survival (PFS: red dotted lines represented 2-4 months PFS expected in this patient group). Right panel shows that vaccination αDC1s loaded with tumor blood vessel antigenic (TBVA) peptides. Example of a near-compete response in a patient with metastatic melanoma who previously progressed on PD1 blockade and received. So far, 4 objective responses (2 nCRs, 2 PR) and 2 SDs (> 9m) ) were seen in 12 pts with PD1-resistant metastatic melanoma. All patients who responded or stabilized developed CTL responses against TBVA but also against melanoma-lineage specific CTL epitopes not included in the vaccine (epitope spreading; Storkus et al.2021). Figures 2A, 2B and 2C show enhanced production of CTL / Th1 / NK cell-attracting chemokines and IL-12p70 and by αDC1 that have been grown and matured for various amount of time. Monocyte cultures were grown for 4 (new protocol) or 6 (traditional protocol) days in the presence of GM-CSF and IL-4 and then matured into αDC1 in IL1β / TNFα / IFNα / IFNγ / poly- I:C for 4h or 18h, before harvesting and washing of DCs. The production of CXCL10 as shown in Figure 2A, CCL22 as shown in Figure 2B, and IL12 / p70 as shown in Figure 2C, were measured by ELISA after 24h of stimulation with (CD40L) or without (DC only) synthetic CD40 ligand. Figure 3 shows the feasibility of selective suppression and activation of the alternative versus canonical pathways of activation of NFkB, using small molecules. DCs were matured with 25ng TNFα for 24 hours, a strong inducer of the canonical NF-κB signaling pathway and DC maturation. NF-κB pathways were selectively modulated using a variety of small molecule inhibitors: NIK-SMI1 alternative NF-κB inhibitor; JSH-23 canonical NF-κB inhibitor; and AZD5582 (SMAC mimetic) alternative and canonical NF-κB “dual” activator. NF-κB signaling and inhibition were determined using imaging flow cytometry to quantify the nuclear translocation of NF-κB proteins p65 (canonical) and p52 (alternative) from the cytoplasm. Because alternative NF-κB is upregulated in later stages of DC maturation after canonical Attorney Docket No: 11390-018WO1 activation, a 30min timepoint was included to validate TNFα as a strong inducer of canonical and not alternative NF-κB. Figures 4A, 4B, 4C and 4D show activation of both canonical and alternative NF-κB pathways during DC maturation extends window of effector function. DCs were matured with either 25ng TNFa or 5nM AZD5582 for indicated timepoints. Figure 4A shows that after maturation, DCs were collected, stained for surface expression of maturation markers (CD80, CD86, CD83, and HLA-DR), then analyzed with flow cytometry. CD83 is used as a representative plot, with the other markers following similar trends. Each condition was analyzed for 50,000 cells. Figures 4B, 4C and 4D show that after maturation for indicated time points, DCs were collected and re-plated with J558-CD40L expressing cells to stimulate IL- 12p70 as shown in Figure 4B, type-1 chemokine production as shown in Figure 4C, and Treg chemokine production as shown in Figure 4D. DCs were plated in a 2:5 ratio DCs:J558 cells and stimulated for 24 hours. Supernatants were collected and analyzed for protein production with ELISA. Each column is mean + SEM of triplicate cultures from one donor. Figure 5 shows that the replacement of poly-I:C with AZD in the αDC1 maturation cocktail enhances IL-12p70 production. DCs were matured with the αDC1 cocktail or with the same cocktail replacing poly-I:C with AZD for 24 hours. DCs were then collected and replated with sCD40L for 24 hours. Supernatants were collected and measured for IL-12p70 production with ELISA. Figures 6A, 6B and 6C show that the selective blockade of alternative pathway of activation of NFkB, using small molecule blocker (but not blockers of canonical NFkB) selectively reduces IDO production but not maturation status nor production of IL-12p70 and desirable chemokines in human DCs. DCs were matured for 24 hours with 25ng TNFα with or without a 1-hour pre-incubation with small molecule inhibitors against canonical NF-κB (JSH- 23) or alternative NF-κB (NIK-SMI1). Figure 6A shows a representative flow cytometry histogram of surface expression of DC maturation marker CD83. Data represents 50,000 cells per condition. Data for CD80, CD86, and HLA-DR follow similar trends as CD83. Figure 6B shows that after maturation, DCs were collected and cultured in a 2:5 ratio with J558-CD40L expressing plasmacytoma cells (to mimic interaction with naïve CD4+T cells) and IFNγ for 24 hours. Supernatants were collected and analyzed for IL-12p70 and chemokines with ELISA. Data shown is mean + SEM of triplicate conditions from one donor. Figure 6C shows that after maturation, DCs were lysed with RLT + beta-mercaptoethanol, and total RNA was isolated using Qiagen RNeasy spin column isolation. Gene expression of typical maturation genes were Attorney Docket No: 11390-018WO1 analyzed with quantitative PCR. Expression Fold Changes are normalized to immature DC controls. Data is mean + SEM of triplicate cultures from one donor. Figures 7A, 7B and 7C show selectively enhanced production of CTL attractants and CTL activators (but not Treg-attracting factor CCL22) by short-term activated alpha DC1s. Alpha-type-1-polarized dendritic cells (αDC1s) were generated three different regimens: the original αDC1 protocol (6days / 18h: Black bars): 6 days of culture in the presence of GM-CSF and IL-4, followed by 18 hours of maturation in αDC1-polarizing cocktail: IL-1b, TNFa, IFNg, IFNa and poly-I:C); short-term-cultured αDC1 protocol (4days / 18h: Light-grey bars: 4 days of culture in the presence of GM-CSF and IL-4, followed by 18 hours of maturation in αDC1- polarizing cocktail; and “4x4”-aDC1 protocol (4days / 18h: Dark-grey bars bars): 6 days of culture in the presence of GM-CSF and IL-4, followed by 18 hours of maturation in αDC1-polarizing cocktail). At the end of maturation, each DC type was harvested, concentration adjusted and replated at the same cell numbers for the additional 24 hours, either in the absence or in their presence of soluble(s) CD40L stimulation. @4 hour supernatants were tested by ELISA for the presence of CXCL10 / IP10 (CTL attractant) as shown in Figure 7A, IL-12p70 (CTL / Th1 / TK cell activator) as shown in Figure 7B, and CCL22 / MDC (Treg attractant) as shown in Figure 7C. “4x4 –αDC1s (4 days culture / 4h maturation) show selectively enhanced ability to CXCL10 (spontaneous and sDC40L-inducible) and (sCD40L-inducible) IL12 / p70, compared to the original αDC1s, without an increase in CCL22 production. The results indicate that just shortening the time of monocyte growth (4 days / 18h) does not contribute to this desirable effect alone, but that the desirable effect is achieved only when shorter times of the initial culture are combined with the shorter maturation time. DETAILED DESCRIPTION Before the present compounds, compositions, articles, devices, and / or methods are disclosed and described, it is to be understood that they are not limited to specific synthetic methods or specific recombinant biotechnology methods unless otherwise specified, or to particular reagents unless otherwise specified, as such may, of course, 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. Definitions As used in the specification and 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 pharmaceutical carrier” includes mixtures of two or more such carriers, and the like. Attorney Docket No: 11390-018WO1 Ranges can be expressed herein as from “about” one particular value, and / or to “about” another particular value. When such a range is expressed, another embodiment includes from the one particular value and / or to the other particular value. Similarly, when values are expressed as approximations, by use of the antecedent “about,” it will be understood that the particular value forms another embodiment. It will be further understood that the endpoints of each of the ranges are significant both in relation to the other endpoint, and independently of the other endpoint. It is also understood that there are a number of values disclosed herein, and that each value is also herein disclosed as “about” that particular value in addition to the value itself. For example, if the value “10” is disclosed, then “about 10” is also disclosed. It is also understood that when a value is disclosed that “less than or equal to” the value, “greater than or equal to the value” and possible ranges between values are also disclosed, as appropriately understood by the skilled artisan. For example, if the value “10” is disclosed the “less than or equal to 10”as well as “greater than or equal to 10” is also disclosed. It is also understood that the throughout the application, data is provided in a number of different formats, and that this data, represents endpoints and starting points, and ranges for any combination of the data points. For example, if a particular data point “10” and a particular data point 15 are disclosed, it is understood that greater than, greater than or equal to, less than, less than or equal to, and equal to 10 and 15 are considered disclosed as well as between 10 and 15. It is also understood that each unit between two particular units are also disclosed. For example, if 10 and 15 are disclosed, then 11, 12, 13, and 14 are also disclosed. In this specification and in the claims which follow, reference will be made to a number of terms which shall be defined to have the following meanings: Optional” or “optionally” means that the subsequently described event or circumstance may or may not occur, and that the description includes instances where said event or circumstance occurs and instances where it does not. An "increase" can refer to any change that results in a greater amount of a symptom, disease, composition, condition or activity. An increase can be any individual, median, or average increase in a condition, symptom, activity, composition in a statistically significant amount. Thus, the increase can be a 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, or 100% increase so long as the increase is statistically significant. A "decrease" can refer to any change that results in a smaller amount of a symptom, disease, composition, condition, or activity. A substance is also understood to decrease the genetic output of a gene when the genetic output of the gene product with the substance is less relative to the output of the gene product without the substance. Also, for example, a decrease Attorney Docket No: 11390-018WO1 can be a change in the symptoms of a disorder such that the symptoms are less than previously observed. A decrease can be any individual, median, or average decrease in a condition, symptom, activity, composition in a statistically significant amount. Thus, the decrease can be a 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, or 100% decrease so long as the decrease is statistically significant. “Effective amount” of an agent refers to a sufficient amount of an agent to provide a desired effect. The amount of agent that is “effective” will vary from subject to subject, depending on many factors such as the age and general condition of the subject, the particular agent or agents, and the like. Thus, it is not always possible to specify a quantified “effective amount.” However, an appropriate “effective amount” in any subject case may be determined by one of ordinary skill in the art using routine experimentation. Also, as used herein, and unless specifically stated otherwise, an “effective amount” of an agent can also refer to an amount covering both therapeutically effective amounts and prophylactically effective amounts. An “effective amount” of an agent necessary to achieve a therapeutic effect may vary according to factors such as the age, sex, and weight of the subject. Dosage regimens can be adjusted to provide the optimum therapeutic response. For example, several divided doses may be administered daily or the dose may be proportionally reduced as indicated by the exigencies of the therapeutic situation. A "pharmaceutically acceptable" component can refer to a component that is not biologically or otherwise undesirable, i.e., the component may be incorporated into a pharmaceutical formulation provided by the disclosure and administered to a subject as described herein without causing significant undesirable biological effects or interacting in a deleterious manner with any of the other components of the formulation in which it is contained. When used in reference to administration to a human, the term generally implies the component has met the required standards of toxicological and manufacturing testing or that it is included on the Inactive Ingredient Guide prepared by the U.S. Food and Drug Administration. "Pharmaceutically acceptable carrier" (sometimes referred to as a “carrier”) means a carrier or excipient that is useful in preparing a pharmaceutical or therapeutic composition that is generally safe and non-toxic and includes a carrier that is acceptable for veterinary and / or human pharmaceutical or therapeutic use. The terms "carrier" or "pharmaceutically acceptable carrier" can include, but are not limited to, phosphate buffered saline solution, water, emulsions (such as an oil / water or water / oil emulsion) and / or various types of wetting agents. As used herein, the term "carrier" encompasses, but is not limited to, any excipient, diluent, filler, salt, buffer, Attorney Docket No: 11390-018WO1 stabilizer, solubilizer, lipid, stabilizer, or other material well known in the art for use in pharmaceutical formulations and as described further herein. “Pharmacologically active” (or simply “active”), as in a “pharmacologically active” derivative or analog, can refer to a derivative or analog (e.g., a salt, ester, amide, conjugate, metabolite, isomer, fragment, etc.) having the same type of pharmacological activity as the parent compound and approximately equivalent in degree. “Therapeutic agent” refers to any composition that has a beneficial biological effect. Beneficial biological effects include both therapeutic effects, e.g., treatment of a disorder or other undesirable physiological condition, and prophylactic effects, e.g., prevention of a disorder or other undesirable physiological condition (e.g., a non-immunogenic cancer). The terms also encompass pharmaceutically acceptable, pharmacologically active derivatives of beneficial agents specifically mentioned herein, including, but not limited to, salts, esters, amides, proagents, active metabolites, isomers, fragments, analogs, and the like. When the terms “therapeutic agent” is used, then, or when a particular agent is specifically identified, it is to be understood that the term includes the agent per se as well as pharmaceutically acceptable, pharmacologically active salts, esters, amides, proagents, conjugates, active metabolites, isomers, fragments, analogs, etc. “Therapeutically effective amount” or “therapeutically effective dose” of a composition (e.g. a composition comprising an agent) refers to an amount that is effective to achieve a desired therapeutic result. In some embodiments, a desired therapeutic result is the control of type I diabetes. In some embodiments, a desired therapeutic result is the control of obesity. Therapeutically effective amounts of a given therapeutic agent will typically vary with respect to factors such as the type and severity of the disorder or disease being treated and the age, gender, and weight of the subject. The term can also refer to an amount of a therapeutic agent, or a rate of delivery of a therapeutic agent (e.g., amount over time), effective to facilitate a desired therapeutic effect, such as pain relief. The precise desired therapeutic effect will vary according to the condition to be treated, the tolerance of the subject, the agent and / or agent formulation to be administered (e.g., the potency of the therapeutic agent, the concentration of agent in the formulation, and the like), and a variety of other factors that are appreciated by those of ordinary skill in the art. In some instances, a desired biological or medical response is achieved following administration of multiple dosages of the composition to the subject over a period of days, weeks, or years. "Inhibit," "inhibiting," and "inhibition" mean to decrease an activity, response, condition, disease, or other biological parameter. This can include but is not limited to the complete Attorney Docket No: 11390-018WO1 ablation of the activity, response, condition, or disease. This may also include, for example, a 10% reduction in the activity, response, condition, or disease as compared to the native or control level. Thus, the reduction can be a 10, 20, 30, 40, 50, 60, 70, 80, 90, 100%, or any amount of reduction in between as compared to native or control levels. By “reduce” or other forms of the word, such as “reducing” or “reduction,” is meant lowering of an event or characteristic (e.g., tumor growth). It is understood that this is typically in relation to some standard or expected value, in other words it is relative, but that it is not always necessary for the standard or relative value to be referred to. For example, “reduces tumor growth” means reducing the rate of growth of a tumor relative to a standard or a control. By “prevent” or other forms of the word, such as “preventing” or “prevention,” is meant to stop a particular event or characteristic, to stabilize or delay the development or progression of a particular event or characteristic, or to minimize the chances that a particular event or characteristic will occur. Prevent does not require comparison to a control as it is typically more absolute than, for example, reduce. As used herein, something could be reduced but not prevented, but something that is reduced could also be prevented. Likewise, something could be prevented but not reduced, but something that is prevented could also be reduced. It is understood that where reduce or prevent are used, unless specifically indicated otherwise, the use of the other word is also expressly disclosed. The term “subject” refers to any individual who is the target of administration or treatment. The subject can be a vertebrate, for example, a mammal. In one aspect, the subject can be human, non-human primate, bovine, equine, porcine, canine, or feline. The subject can also be a guinea pig, rat, hamster, rabbit, mouse, or mole. Thus, the subject can be a human or veterinary patient. The term “patient” refers to a subject under the treatment of a clinician, e.g., physician. The term “therapeutically effective” refers to the amount of the composition used is of sufficient quantity to ameliorate one or more causes or symptoms of a disease or disorder. Such amelioration only requires a reduction or alteration, not necessarily elimination. The term “treatment” refers to the medical management of a patient with the intent to cure, ameliorate, stabilize, or prevent a disease, pathological condition, or disorder. This term includes active treatment, that is, treatment directed specifically toward the improvement of a disease, pathological condition, or disorder, and also includes causal treatment, that is, treatment directed toward removal of the cause of the associated disease, pathological condition, or disorder. In addition, this term includes palliative treatment, that is, treatment designed for the relief of symptoms rather than the curing of the disease, pathological condition, or disorder; Attorney Docket No: 11390-018WO1 preventative treatment, that is, treatment directed to minimizing or partially or completely inhibiting the development of the associated disease, pathological condition, or disorder; and supportive treatment, that is, treatment employed to supplement another specific therapy directed toward the improvement of the associated disease, pathological condition, or disorder. "Comprising" is intended to mean that the compositions, methods, etc. include the recited elements, but do not exclude others. "Consisting essentially of'' when used to define compositions and methods, shall mean including the recited elements, but excluding other elements of any essential significance to the combination. Thus, a composition consisting essentially of the elements as defined herein would not exclude trace contaminants from the isolation and purification method and pharmaceutically acceptable carriers, such as phosphate buffered saline, preservatives, and the like. "Consisting of'' shall mean excluding more than trace elements of other ingredients and substantial method steps for administering the compositions provided and / or claimed in this disclosure. Embodiments defined by each of these transition terms are within the scope of this disclosure. A “control” is an alternative subject or sample used in an experiment for comparison purposes. A control can be "positive" or "negative." “Culture” or “cell culture” is the process by which cells are grown under controlled conditions, generally outside their natural environment. After the cells of interest have been isolated from living tissue, they can subsequently be maintained under carefully controlled conditions. These conditions vary for each cell type, but generally consist of a suitable vessel with a substrate or medium that supplies the essential nutrients (amino acids, carbohydrates, vitamins, minerals), growth factors, hormones, and gases (CO2, O2), and regulates the physio-chemical environment (pH buffer, osmotic pressure, temperature). Most cells require a surface or an artificial substrate to form an adherent culture as a monolayer (one single-cell thick), whereas others can be grown free floating in a medium as a suspension culture. "Cell culture" also refers to the culturing of cells derived from multicellular eukaryotes, especially animal cells, in contrast with other types of culture that also grow cells, such as plant tissue culture, fungal culture, and microbiological culture (of microbes). “Inhibitors” or “antagonist” of expression or of activity are used to refer to inhibitory molecules, respectively, identified using in vitro and in vivo assays for expression or activity of a described target protein, e.g., ligands, antagonists, and their homologs and mimetics. Inhibitors are agents that, e.g., inhibit expression or bind to, partially or totally block stimulation or activity, decrease, prevent, delay activation, inactivate, desensitize, or down regulate the activity of the described target protein, e.g., antagonists. Control samples (untreated with inhibitors) are Attorney Docket No: 11390-018WO1 assigned a relative activity value of 100%. Inhibition of a described target protein is achieved when the activity value relative to the control is about 80%, optionally 50% or 25, 10%, 5%, or 1% or less. The term “administer,” “administering”, or derivatives thereof refer to delivering a composition, substance, inhibitor, or medication to a subject or object by one or more the following routes: oral, topical, intravenous, subcutaneous, transcutaneous, transdermal, intramuscular, intra-joint, parenteral, intra-arteriole, intradermal, intraventricular, intracranial, intraperitoneal, intralesional, intranasal, rectal, vaginal, by inhalation or via an implanted reservoir. The term “parenteral” includes subcutaneous, intravenous, intramuscular, intra- articular, intra-synovial, intrasternal, intrathecal, intrahepatic, intralesional, and intracranial injections or infusion techniques. A “vaccine” refers to a biological preparation that provides active acquired immunity to a particular infectious diseases caused by a virus, bacteria, parasite, or any other microorganisms. Vaccines typically comprise an agent or several agents, also referred to as antigens, resembling the disease-causing microorganism and is often made from weakened or killed forms of the microbe, its toxins, or its surface proteins / peptides. Vaccines are also made to comprise additional components, such as adjuvants, preservatives, and / or stabilizers to boost the immune response, improve safety, and improve vaccine storage. The terms “anticancer” and “anticarcinogen” refers to a substance, composition, or formula that counteracts the effects or inhibits the development of a cancerous cells and tissues. The term “cancer” is used to address any neoplastic disease, and is not limited to epithelial neoplasms (surface and glandular cancers; such a squamous cancers or adenomas)). It is used here to describe both solid tumors and hematologic malignancies, including epithelial (surface and glandular) cancers, soft tissue and bone sarcomas, angiomas, mesothelioma, melanoma, lymphomas, leukemias and myeloma. The terms "cell," "cell line" and "cell culture" include progeny. It is also understood that all progenies may not be precisely identical in DNA content, due to deliberate or inadvertent mutations. Variant progeny that have the same function or biological property, as screened for in the originally transformed cell, are included. The "host cells" used in the present invention generally are prokaryotic or eukaryotic hosts. A “T cell” refers to a type of lymphocyte that is one of the most important white blood cells of the immune system. T cells can be distinguished from other lymphocytes by the presence of a T-cell receptor (TCR) on their cell surface. The immune-mediated cell death function of T cells is carried by two major subtypes: CD8+“killer” T cells and CD4+“helper T cells. Attorney Docket No: 11390-018WO1 An “epitope” or “antigenic determinant” refer to the part of an antigen, a molecular structure, or foreign particulate that can bind to a specific antibody or T-cell receptor. The presence of antigens or epitopes of antigens within a host can illicit an immune response. An “antigen” refers to a molecule, moiety, foreign particulate matter, or an allergen that can bind to a specific antibody or T cell receptor. The presence of antigens within a host can illicit an immune response against said molecule, moiety, foreign particulate matter, or allergen. Throughout this application, various publications are referenced. The disclosures of these publications in their entireties are hereby incorporated by reference into this application in order to more fully describe the state of the art to which this pertains. The references disclosed are also individually and specifically incorporated by reference herein for the material contained in them that is discussed in the sentence in which the reference is relied upon. Method of making short-term-matured alpha-type 1-dendritic (ST-αDC1) cells In one aspect disclosed herein, is a method of making one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (including, but not limited to 4x4 short-term-matured alpha-type 1-dendritic (4x4 ST-αDC1)). A dendritic cells (DC) is a type of immune cell that play a key role in the body's immune response. DCs are antigen-presenting cells (APCs) that sense, process, and present antigens to other immune cells, such as T lymphocytes. This process helps to initiate and regulate the body's immune response. DCs are found in tissues throughout the body of a subject and are derived from hematopoietic stem cells (HSCs) in the bone marrow. DCs play a role in many diseases, including cancer, autoimmune disease, viral infections, and allergic diseases. DC function can be modulated to improve cancer immunotherapy and treat other diseases. For example, DC-based vaccines are one strategy being developed. The method disclosed herein comprises culturing one or more monocytic cell(s), obtained from peripheral blood of a subject with GM-CSF, IL-4 or a combination thereof, for about 4 days to make one or more immature DC cell(s). In some embodiments, one or more monocytic cell(s) are cultures in the presence of at least one type-1 IFN (IFNα or IFNβ) and type-2 IFN (IFNγ). In some embodiments, one or more monocytic cell(s) are cultured for about 1, 2, 3, 4 days. In some embodiments, one or more monocytic cell(s) are cultured for 1 day. In some embodiments, one or more monocytic cell(s) are cultured for 2 days. In some embodiments, one or more monocytic cell(s) are cultured for 3 days. In some embodiments, one or more monocytic cell(s) are cultured for 4 days. In some embodiments, one or more monocytic Attorney Docket No: 11390-018WO1 cell(s) are cultured for 5 days. In some embodiments, one or more monocytic cell(s) are cultured for 6 days. Thereafter, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail (comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C)) formulated in a unitary composition or maintained separately) for less than 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for between 2 and 18 hours, between 2 and 14 hours, between 2 and 10 hours, between 2 and 8 hours, between 2 and 6 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for 4 hours. Accordingly in some aspects, disclosed herein are methods of making ST-αDC1 wherein the one or more monocytic cell(s) are cultured for 4 days and the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for 4 hours. When the culturing is 4 days and the cell maturation cocktail exposure is 4 hours, the the ST αDC1 cell are referred to as 4x4 ST αDC1. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, Attorney Docket No: 11390-018WO1 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml. In some embodiments, the Interferon α (IFNα) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml. In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, Attorney Docket No: 11390-018WO1 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). Some other exemplary inhibitors of TGF-β signaling include but are not limited to tranilast, losartan, glitazones, and imatinib mesylate, pirfenidone, halofuginone, trabedersen (AP 12009), galunisertib (LY2157299), vactosertib (TEW-7197), LSKL, tnhibitor of thrombospondin (TSP-1), cilengitide, M200, NIS793, fresolimumab (GC1008), AVID200, or ABBV-151. In some embodiments, the one or more the ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1cells) produces at least 50% increased IL-12p70 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). Interleukin 12 (termed IL-12p70) is an important immunoregulatory cytokine that is produced mainly by antigen-presenting cells. The expression of IL-12 during infection regulates innate responses and determines the type of adaptive immune responses. IL-12 induces interferon-γ (IFN-γ) production and triggers CD4+T cells to differentiate into type 1 T helper (Th1) cells. In some embodiments, the one or more 4x4 ST- Attorney Docket No: 11390-018WO1 αDC1 cell(s) produces at least 50%, 51%, 52%, 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% increased IL-12p70 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). CD40L is a membrane glycoprotein expressed on activated T cells, B cells, platelets, and other cells. As disclosed herein, CD40L is a co- stimulatory molecule that binds to CD40, a transmembrane protein on other cells, to amplify the immune response and produce antibodies. CD40L signaling induces a cascade that activates CD4 T cells, which then further induce CD40L expression. In some embodiments, the ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1cells) are stimulated with synthetic CD40 ligand (CD40L) for about 24 hours. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1cells) produces at least 50% increased CXCL10 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). CXCL10, also known as interferon-gamma-induced protein 10 (IP-10) or small-inducible cytokine B10, is a protein that plays a role in immune responses and perpetuating inflammation. In some embodiments, the one or more 4x4 ST-αDC1 cell(s) produces at least 50%, 51%, 52%, 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% increased CXCL10 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1cells) produces at least 50% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). CCL22 also known as monocyte chemotactic protein 1 (MCP-1), promotes tumors in human cancers. It plays a role in recruiting T-reg cells and infiltrating macrophages. CCL22 is a chemokine that helps regulate immunity by promoting communication between regulatory T cells (Tregs) and dendritic cells in lymph nodes. As disclosed herein, the decrease in CCL22 can inhibit the migration of regulatory T cells, reduce immunosuppression, increase anti-tumor immune responses and block cancer progression. In some embodiments, the one or more 4x4 ST-αDC1 cell(s) produces at least 50%, 51%, 52%, Attorney Docket No: 11390-018WO1 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). Method of treating a pre-cancerous, cancerous, or metastatic condition It is understood and herein contemplated that the disclosed ST-αDC1cells (including, but not limited to 4x4 ST-αDC1cells) are useful in the treatment of pre-cancerous, cancerous, and metastatic conditions. Exemplary cancers include, but are not limited to, acoustic neuroma, adenocarcinoma, adrenal gland cancer, anal cancer, angiosarcoma (e.g., lymphangiosarcoma, lymphangioendotheliosarcoma, hemangiosarcoma), appendix cancer, benign monoclonal gammopathy, biliary cancer (e.g., cholangiocarcinoma), bladder cancer, breast cancer (e.g., adenocarcinoma of the breast, papillary carcinoma of the breast, mammary cancer, medullary carcinoma of the breast), brain cancer (e.g., meningioma; glioma, e.g., astrocytoma, oligodendroglioma; medulloblastoma), bronchus cancer, carcinoid tumor, cervical cancer (e.g., cervical adenocarcinoma), choriocarcinoma, chordoma, craniopharyngioma, colorectal cancer (e.g., colon cancer, rectal cancer, colorectal adenocarcinoma), epithelial carcinoma, ependymoma, endotheliosarcoma (e.g., Kaposi's sarcoma, multiple idiopathic hemorrhagic sarcoma), endometrial cancer (e.g., uterine cancer, uterine sarcoma), esophageal cancer (e.g., adenocarcinoma of the esophagus, Barrett's adenocarinoma), Ewing's sarcoma, eye cancer (e.g., intraocular melanoma, retinoblastoma), familiar hypereosinophilia, gall bladder cancer, gastric cancer (e.g., stomach adenocarcinoma), gastrointestinal stromal tumor (GIST), head and neck cancer (e.g., head and neck squamous cell carcinoma, oral cancer (e.g., oral squamous cell carcinoma (OSCC), throat cancer (e.g., laryngeal cancer, pharyngeal cancer, nasopharyngeal cancer, oropharyngeal cancer)), hematopoietic cancers (e.g., leukemia such as acute lymphocytic leukemia (ALL) (e.g., B-cell ALL, T-cell ALL), acute myelocytic leukemia (AML) (e.g., B-cell AML, T-cell AML), chronic myelocytic leukemia (CML) (e.g., B-cell CML, T-cell CML), and chronic lymphocytic leukemia (CLL) (e.g., B-cell CLL, T-cell CLL); lymphoma such as Hodgkin lymphoma (HL) (e.g., B-cell HL, T-cell HL) and non-Hodgkin lymphoma (NHL) (e.g., B-cell NHL such as diffuse large cell lymphoma (DLCL) (e.g., diffuse large B-cell lymphoma (DLBCL)), follicular lymphoma, chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL / SLL), mantle cell lymphoma (MCL), marginal zone B-cell lymphomas (e.g., mucosa- Attorney Docket No: 11390-018WO1 associated lymphoid tissue (MALT) lymphomas, nodal marginal zone B-cell lymphoma, splenic marginal zone B-cell lymphoma), primary mediastinal B-cell lymphoma, Burkitt lymphoma, lymphoplasmacytic lymphoma (i.e., “Waldenstrom's macroglobulinemia”), hairy cell leukemia (HCL), immunoblastic large cell lymphoma, precursor B-lymphoblastic lymphoma and primary central nervous system (CNS) lymphoma; and T-cell NHL such as precursor T-lymphoblastic lymphoma / leukemia, peripheral T-cell lymphoma (PTCL) (e.g., cutaneous T-cell lymphoma (CTCL) (e.g., mycosis fungiodes, Sezary syndrome), angioimmunoblastic T-cell lymphoma, extranodal natural killer T-cell lymphoma, enteropathy type T-cell lymphoma, subcutaneous panniculitis-like T-cell lymphoma, anaplastic large cell lymphoma); a mixture of one or more leukemia / lymphoma as described above; and multiple myeloma (MM)), heavy chain disease (e.g., alpha chain disease, gamma chain disease, mu chain disease), hemangioblastoma, inflammatory myofibroblastic tumors, immunocytic amyloidosis, kidney cancer (e.g., nephroblastoma a.k.a. Wilms' tumor, renal cell carcinoma), liver cancer (e.g., hepatocellular cancer (HCC), malignant hepatoma), lung cancer (e.g., bronchogenic carcinoma, small cell lung cancer (SCLC), non-small cell lung cancer (NSCLC), adenocarcinoma of the lung), leiomyosarcoma (LMS), mastocytosis (e.g., systemic mastocytosis), myelodysplastic syndrome (MDS), mesothelioma, myeloproliferative disorder (MPD) (e.g., polycythemia Vera (PV), essential thrombocytosis (ET), agnogenic myeloid metaplasia (AMM) a.k.a. myelofibrosis (MF), chronic idiopathic myelofibrosis, chronic myelocytic leukemia (CML), chronic neutrophilic leukemia (CNL), hypereosinophilic syndrome (HES)), neuroblastoma, neurofibroma (e.g., neurofibromatosis (NF) type 1 or type 2, schwannomatosis), neuroendocrine cancer (e.g., gastroenteropancreatic neuroendoctrine tumor (GEP-NET), carcinoid tumor), osteosarcoma, ovarian cancer (e.g., cystadenocarcinoma, ovarian embryonal carcinoma, ovarian adenocarcinoma), papillary adenocarcinoma, pancreatic cancer (e.g., pancreatic adenocarcinoma, intraductal papillary mucinous neoplasm (IPMN), Islet cell tumors), penile cancer (e.g., Paget's disease of the penis and scrotum), pinealoma, primitive neuroectodermal tumor (PNT), prostate cancer (e.g., prostate adenocarcinoma), rectal cancer, rhabdomyosarcoma, salivary gland cancer, skin cancer (e.g., squamous cell carcinoma (SCC), keratoacanthoma (KA), melanoma, basal cell carcinoma (BCC)), small bowel cancer (e.g., appendix cancer), soft tissue sarcoma (e.g., malignant fibrous histiocytoma (MFH), liposarcoma, malignant peripheral nerve sheath tumor (MPNST), chondrosarcoma, fibrosarcoma, myxosarcoma), sebaceous gland carcinoma, sweat gland carcinoma, synovioma, testicular cancer (e.g., seminoma, testicular embryonal carcinoma), thyroid cancer (e.g., papillary carcinoma of the thyroid, papillary thyroid carcinoma (PTC), medullary thyroid cancer), urethral cancer, vaginal cancer and vulvar cancer (e.g., Paget's disease Attorney Docket No: 11390-018WO1 of the vulva). Accordingly, disclosed herein, are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition (such as, for example, glioma, brain cancer (including, but not limited to recurrent brain cancer), anaplastic astrocytoma (AA), and melanoma (including, but not limited to checkpoint-resistant metastatic melanoma)) in a subject comprising; administering to the subject a therapeutically effective amount of one or more short-term-matured alpha-type 1-dendritic (ST- αDC1) cell(s) (including, but not limited to 4x4 ST-αDC1) made by the any method disclosed herein. For example, disclosed herein are methods of treating, inhibiting, reducing, decreasing, ameliorating, and / or preventing a pre-cancerous, cancerous, and / or metastatic condition (such as, for example, glioma, brain cancer (including, but not limited to recurrent brain cancer), anaplastic astrocytoma (AA), and melanoma (including, but not limited to checkpoint-resistant metastatic melanoma)) in a subject comprising; administering to the subject a therapeutically effective amount of one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s) (including, but not limited to 4x4 ST-αDC1), wherein the one or more ST-αDC1 cell(s) are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C), for less than 18 hours, resulting in the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1). In some embodiments the method disclosed herein comprises administering to the subject a therapeutically effective amount of one or more of any of the short-term-matured alpha-type 1-dendritic cell(s) disclosed herein, wherein the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s). In one aspect disclosed herein, is a method of treating a pre-cancerous or cancerous condition in a subject comprising a) isolating one or more T cell(s) from the subject, b) sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST- αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) ex vivo, wherein the one or more ex vivo-sensitized T cell(s); and c) administering to a subject in need thereof, the one or more ex vivo-sensitized T cell(s), wherein the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) are made by a method comprising, culturing one or more monocytic cell(s) with Attorney Docket No: 11390-018WO1 GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s). In some embodiments, one or more monocytic cell(s) are cultures in the presence of at least one type-1 IFN (IFNα or IFNβ) and type-2 IFN (IFNγ). In some embodiments, one or more monocytic cell(s) are cultured for about 1, 2, 3, 4 days. In some embodiments, one or more monocytic cell(s) are cultured for 1 day. In some embodiments, one or more monocytic cell(s) are cultured for 2 days. In some embodiments, one or more monocytic cell(s) are cultured for 3 days. In some embodiments, one or more monocytic cell(s) are cultured for 4 days. In some embodiments, one or more monocytic cell(s) are cultured for 5 days. In some embodiments, one or more monocytic cell(s) are cultured for 6 days. Thereafter, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail (comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C)) formulated in a unitary composition or maintained separately) for less than 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for between 2 and 18 hours, between 2 and 14 hours, between 2 and 10 hours, between 2 and 8 hours, between 2 and 6 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for 4 hours. Accordingly in some aspects, disclosed herein are methods of making ST-αDC1 wherein the one or more monocytic cell(s) are cultured for 4 days and the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for 4 hours. When the culturing is 4 days and the cell maturation cocktail exposure is 4 hours, the ST αDC1 cell are referred to as 4x4 ST αDC1. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, Attorney Docket No: 11390-018WO1 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml. In some embodiments, the Interferon α (IFNα) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml. Attorney Docket No: 11390-018WO1 In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is loaded with at least one or more antigenic peptides. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is loaded with six antigenic peptides targeting tumor-associated blood vessel antigens (TBVA) (such as, for example, DLK1, EphA2, HBB, NRP1, RGS5, TEM1) uniformly expressed on blood vessels of multiple human tumors. Some exemplary tumor antigenic peptides include but are not limited to, Attorney Docket No: 11390-018WO1 BAGE-1, CT37 / FMR1NB, Cyclin-A1, Cyclin-A1, D393-CD20n, GAGE-1,2,8, GAGE-3,4,5,6,7, GnTV, HERV-E, HERV-K-MEL, KK-LC-1, KM-HN-1, LAGE-1, LRPAP1, LY6K, MAGE-A1, MAGE-A10, MAGE-A12 m, MAGE-A2, MAGE-A3, MAGE-A4, MAGE-A6, MAGE-A9, MAGE-C1, MAGE-C2, mucin, NA88-A, NY-ESO-1 / LAGE-2, NY-ESO-1 / LAGE-2, SAGE, Sp17, SSX-2, SSX-4, TAG-1, TAG-2, TRAG-3, TRP2-INT2, XAGE-1b / GAGED2. In some embodiments, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). Some other exemplary inhibitors of TGF-β signaling include but are not limited to tranilast, losartan, glitazones, and imatinib mesylate, pirfenidone, halofuginone, trabedersen (AP 12009), galunisertib (LY2157299), vactosertib (TEW-7197), LSKL, tnhibitor of thrombospondin (TSP-1), cilengitide, M200, NIS793, fresolimumab (GC1008), AVID200, or ABBV-151. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1)produces at least 50% increased IL-12p70 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more 4x4 ST-αDC1 cell(s) produces at least 50%, 51%, 52%, 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% increased IL-12p70 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) produces at least 50% increased CXCL10 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more 4x4 ST-αDC1 cell(s) produces at least 50%, 51%, 52%, 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% increased CXCL10 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1)produces at least 50% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation Attorney Docket No: 11390-018WO1 with synthetic CD40 ligand (CD40L). In some embodiments, the one or more 4x4 ST-αDC1 cell(s) produces at least 50%, 51%, 52%, 53%, 54%, 55%, 56%, 57%, 58%, 59%, 60%, 61%, 62%, 63%, 64%, 65%, 66%, 67%, 68%, 69%, 70%, 71%, 72%, 73%, 74%, 75%, 76%, 77%, 78%, 79%, 80%, 81%, 82%, 83%, 84%, 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or 100% decreased Treg chemokine CCL22, compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L). In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) increases intratumoral accumulation of cytotoxic T lymphocytes (CTLs) compared to a control and sensitizes tumors to cancer therapy such as, for example, anti-PD1 therapy. In some embodiments, the cancer therapy can be but is not limited to an immunotherapy, hormone therapy, targeted therapy such as, for example, chemotherapy. Anti-cancer agents encompass biotherapeutic anti-cancer agents as well as chemotherapeutic agents. Exemplary biotherapeutic anti-cancer agents include, but are not limited to, interferons, cytokines (e.g., tumor necrosis factor, interferon α, interferon γ), vaccines, hematopoietic growth factors, monoclonal serotherapy, immunostimulants and / or immunodulatory agents (e.g., IL-1, 2, 4, 6, or 12), immune cell growth factors (e.g., GM-CSF) and antibodies (e.g. HERCEPTIN (trastuzumab), T-DM1, AVASTIN (bevacizumab), ERBITUX (cetuximab), VECTIBIX (panitumumab), RITUXAN (rituximab), BEXXAR (tositumomab)). Exemplary chemotherapeutic agents include, but are not limited to, anti-estrogens (e.g. tamoxifen, raloxifene, and megestrol), LHRH agonists (e.g. goscrclin and leuprolide), anti- androgens (e.g. flutamide and bicalutamide), photodynamic therapies (e.g. vertoporfin (BPD- MA), phthalocyanine, photosensitizer Pc4, and demethoxy-hypocrellin A (2BA-2-DMHA)), nitrogen mustards (e.g. cyclophosphamide, ifosfamide, trofosfamide, chlorambucil, estramustine, and melphalan), nitrosoureas (e.g. carmustine (BCNU) and lomustine (CCNU)), alkylsulphonates (e.g. busulfan and treosulfan), triazenes (e.g. dacarbazine, temozolomide), platinum containing compounds (e.g. cisplatin, carboplatin, oxaliplatin), vinca alkaloids (e.g. vincristine, vinblastine, vindesine, and vinorelbine), taxoids (e.g. paclitaxel or a paclitaxel equivalent such as nanoparticle albumin-bound paclitaxel (ABRAXANE), docosahexaenoic acid bound-paclitaxel (DHA-paclitaxel, Taxoprexin), polyglutamate bound-paclitaxel (PG-paclitaxel, paclitaxel poliglumex, CT-2103, XYOTAX), the tumor-activated prodrug (TAP) ANG1005 (Angiopep-2 bound to three molecules of paclitaxel), paclitaxel-EC-1 (paclitaxel bound to the erbB2-recognizing peptide EC-1), and glucose-conjugated paclitaxel, e.g., 2′-paclitaxel methyl 2- glucopyranosyl succinate; docetaxel, taxol), epipodophyllins (e.g. etoposide, etoposide Attorney Docket No: 11390-018WO1 phosphate, teniposide, topotecan, 9-aminocamptothecin, camptoirinotecan, irinotecan, crisnatol, mytomycin C), anti-metabolites, DHFR inhibitors (e.g. methotrexate, dichloromethotrexate, trimetrexate, edatrexate), IMP dehydrogenase inhibitors (e.g. mycophenolic acid, tiazofurin, ribavirin, and EICAR), ribonucleotide reductase inhibitors (e.g. hydroxyurea and deferoxamine), uracil analogs (e.g.5-fluorouracil (5-FU), floxuridine, doxifluridine, ratitrexed, tegafur-uracil, capecitabine), cytosine analogs (e.g. cytarabine (ara C), cytosine arabinoside, and fludarabine), purine analogs (e.g. mercaptopurine and Thioguanine), Vitamin D3 analogs (e.g. EB 1089, CB 1093, and KH 1060), isoprenylation inhibitors (e.g. lovastatin), dopaminergic neurotoxins (e.g. 1-methyl-4-phenylpyridinium ion), cell cycle inhibitors (e.g. staurosporine), actinomycin (e.g. actinomycin D, dactinomycin), bleomycin (e.g. bleomycin A2, bleomycin B2, peplomycin), anthracycline (e.g. daunorubicin, doxorubicin, pegylated liposomal doxorubicin, idarubicin, epirubicin, pirarubicin, zorubicin, mitoxantrone), MDR inhibitors (e.g. verapamil), Ca2+ATPase inhibitors (e.g. thapsigargin), imatinib, thalidomide, lenalidomide, tyrosine kinase inhibitors (e.g., axitinib (AG013736), bosutinib (SKI-606), cediranib (RECENTIN™, AZD2171), dasatinib (SPRYCEL®, BMS-354825), erlotinib (TARCEVA®), gefitinib (IRESSA®), imatinib (Gleevec®, CGP57148B, STI-571), lapatinib (TYKERB®, TYVERB®), lestaurtinib (CEP-701), neratinib (HKI-272), nilotinib (TASIGNA®), semaxanib (semaxinib, SU5416), sunitinib (SUTENT®, SU11248), toceranib (PALLADIA®), vandetanib (ZACTIMA®, ZD6474), vatalanib (PTK787, PTK / ZK), trastuzumab (HERCEPTIN®), bevacizumab (AVASTIN®), rituximab (RITUXAN®), cetuximab (ERBITUX®), panitumumab (VECTIBIX®), ranibizumab (Lucentis®), nilotinib (TASIGNA®), sorafenib (NEXAVAR®), everolimus (AFINITOR®), alemtuzumab (CAMPATH®), gemtuzumab ozogamicin (MYLOTARG®), temsirolimus (TORISEL®), ENMD-2076, PCI-32765, AC220, dovitinib lactate (TKI258, CHIR-258), BIBW 2992 (TOVOK™), SGX523, PF-04217903, PF-02341066, PF-299804, BMS-777607, ABT-869, MP470, BIBF 1120 (VARGATEF®), AP24534, JNJ-26483327, MGCD265, DCC-2036, BMS- 690154, CEP-11981, tivozanib (AV-951), OSI-930, MM-121, XL-184, XL-647, and / or XL228), proteasome inhibitors (e.g., bortezomib (VELCADE)), mTOR inhibitors (e.g., rapamycin, temsirolimus (CCI-779), everolimus (RAD-001), ridaforolimus, AP23573 (Ariad), AZD8055 (AstraZeneca), BEZ235 (Novartis), BGT226 (Norvartis), XL765 (Sanofi Aventis), PF-4691502 (Pfizer), GDC0980 (Genetech), SF1126 (Semafoe) and OSI-027 (OSI)), oblimersen, gemcitabine, caminomycin, leucovorin, pemetrexed, cyclophosphamide, dacarbazine, procarbizine, prednisolone, dexamethasone, campathecin, plicamycin, asparaginase, aminopterin, methopterin, porfiromycin, melphalan, leurosidine, leurosine, chlorambucil, trabectedin, procarbazine, discodermolide, caminomycin, aminopterin, and hexamethyl melamine. Attorney Docket No: 11390-018WO1 The one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) may be administered in such amounts, time, and route deemed necessary in order to achieve the desired result. The exact amount of the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) will vary from subject to subject, depending on the species, age, and general condition of the subject, the severity of the cancer, the particular one or more ST-αDC1 cell(s), its mode of administration, its mode of activity, and the like. The one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is preferably formulated in dosage unit form for ease of administration and uniformity of dosage. It will be understood, however, that the total daily usage of the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) will be decided by the attending physician within the scope of sound medical judgment. The specific therapeutically effective dose level for any particular subject will depend upon a variety of factors including the cancer being treated and the severity of the cancer; the activity of the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) employed; the age, body weight, general health, sex and diet of the patient; the time of administration, route of administration, and the duration of the treatment; drugs used in combination or coincidental with the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) employed; and like factors well known in the medical arts. The one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) may be administered by any route. In some embodiments, the one or more ST-αDC1 cell(s) is administered via a variety of routes, including, intravenous, intramuscular, intra-arterial, intramedullary, intrathecal, subcutaneous, intraventricular, transdermal, interdermal, rectal, intravaginal, intraperitoneal, topical (as by powders, ointments, creams, and / or drops), mucosal, nasal, buccal, enteral, sublingual; by intratracheal instillation, bronchial instillation, and / or inhalation; and / or as an oral spray, nasal spray, and / or aerosol. In general, the most appropriate route of administration will depend upon a variety of factors including the nature of the composition (e.g., its stability in the environment of the gastrointestinal tract), the condition of the subject (e.g., whether the subject is able to tolerate oral administration), etc. In some embodiments, the one or more 4x4 ST-αDC1 cell(s) are administered to the subject as a systemic injection, intratumorally or within a peritumoral intracavity. The exact amount of the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) required to achieve a therapeutically or prophylactically effective amount will vary from subject to subject, depending on species, age, and general condition of a subject, severity of the side effects, identity of the particular compound(s), mode of administration, and the like. The amount to be administered to, for example, a child or an adolescent can be determined by a medical Attorney Docket No: 11390-018WO1 practitioner or person skilled in the art and can be lower or the same as that administered to an adult. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is administered to the subject 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, or more times. In some embodiments, the the one or more ST-αDC1 cell(s) is administered to the subject daily. In some embodiments, the the one or more ST-αDC1 cell(s) is administered to the subject every day, every 2 days, every 3 days, every 4 days, every 5 days, every 6 days, every 7 days, or more. In some embodiments, the one or more ST-αDC1 cell(s(including, but not limited to 4x4 ST-αDC1)) is administered to the subject is administered every week, every 2 weeks, every 3 weeks, every 4 weeks, or more. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is administered to the subject every month, every 2 months, every 3 months, every 4 months, every 5 months, every 6 months, every 7 months, every 8 months, every 9 months, every 10 months, every 11 months, every 12 months, or more. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is administered to the subject every year, every 2 years, every 3 years, every 4 years, every 5 years, or more. In some embodiments, the method further comprises isolating one or more T cells from the subject, sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) ex vivo, and administering to the subject, the one or more ex vivo-sensitized T cell(s). Composition of an adoptive cell therapy In one aspect disclosed herein is an adoptive cell therapy comprising one or more ST- αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) and / or one or more in vitro or ex vivo- sensitized T cell(s). In some embodiments, the one or more in vitro or ex vivo-sensitized T cell(s) is activated by one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1), which are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s). In some embodiments, one or more monocytic cell(s) are cultures in the presence of at least one type-1 IFN (IFNα or IFNβ) and type-2 IFN (IFNγ). In some embodiments, one or more monocytic cell(s) are cultured for about 1, 2, 3, 4 days. In some embodiments, one or more monocytic Attorney Docket No: 11390-018WO1 cell(s) are cultured for 1 day. In some embodiments, one or more monocytic cell(s) are cultured for 2 days. In some embodiments, one or more monocytic cell(s) are cultured for 3 days. In some embodiments, one or more monocytic cell(s) are cultured for 4 days. In some embodiments, one or more monocytic cell(s) are cultured for 5 days. In some embodiments, one or more monocytic cell(s) are cultured for 6 days. Thereafter, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail (comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand (such as, for example, Polyinosinic:polycytidylic acid (poly-I:C)) formulated in a unitary composition or maintained separately) for less than 18 hours, resulting in the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1). In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 1 hour. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 2 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 3 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 5 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 6 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 7 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 8 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 9 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 10 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 11 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 12 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 13 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 14 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 15 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 16 hours. In some Attorney Docket No: 11390-018WO1 embodiments the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 17 hours. In some embodiments the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 18 hours. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for 4 hours. In some embodiments, one or more monocytic cell(s) are cultures for 4 days. In some embodiments, the one or more immature DC cell(s) are exposed to the αDC1 cell maturation cocktail for about 4 hours or for 4 hours. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Interleukin 1β (IL1β) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml. In some embodiments, the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml. Attorney Docket No: 11390-018WO1 In some embodiments, the Interferon α (IFNα) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml. In some embodiments, the Interferon γ (IFNγ) is at a concentration of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 110, 120, 130, 140, 150, 160, 170, 180, 190, 200, 210, 220, 230, 240, 250, 260, 270, 280, 290, 300, 310, 320, 330, 340, 350, 360, 370, 380, 390, 400, 410, 420, 430, 440, 450, 460, 470, 480, 490, 500, 510, 520, 530, 540, 550, 560, 570, 580, 590, 600, 610, 620, 630, 640, 650, 660, 670, 680, 690, 700, 710, 720, 730, 740, 750, 760, 770, 780, 790, 800, 810, 820, 830, 840, 850, 860, 870, 890, 900, 910, 920, 930, 940, 950, 960, 970, 980, 990, 1000, 1100, 1200, 1300, 1400, 1500, 1600, 1700, 1800, 1900, 2000, 2100, 2200, 2300, 2400, 2500, 2600, 2700, 2800, 2900, 3000, 3100, 3200, 3300, 3400, 3500, 3600, 3700, 3800, 3900, 4000, 4100, 4200, 4300, 4400, 4500, 4600, 4700, 4800, 4900, 5000, 5100, 5200, 5300, 5400, 5500, 5600, 5700, 5800, 5900, 6000, 6100, 6200, 6300, 6400, 6500, 6600, 6700, 6800, 6900, 7000, 7100, 7200, 7300, 7400, 7500, 7600, 7700, 7800, 7900, 8000, 8100, 8200, 8300, 8400, 8500, 8600, 8700, 8800, 8900, 9000, 9100, 9200, 9300, 9400, 9500, 9600, 9700, 9800, or 10,000 U / ml. Attorney Docket No: 11390-018WO1 In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of 0.2 ng / ml - 200 μg / ml. In some embodiments, the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121, 122, 123, 124, 125, 126, 127, 128, 129, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 198, 199, or 200 ng / ml. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is loaded with at least one or more antigenic peptides. In some embodiments, the one or more ST-αDC1 cell(s) (including, but not limited to 4x4 ST-αDC1) is loaded with six antigenic peptides targeting tumor-associated blood vessel antigens (TBVA) (such as, for example, DLK1, EphA2, HBB, NRP1, RGS5, TEM1) uniformly expressed on blood vessels of multiple human tumors. Some exemplary tumor antigenic peptides include but are not limited to, BAGE-1, CT37 / FMR1NB, Cyclin-A1, Cyclin-A1, D393-CD20n, GAGE-1,2,8, GAGE-3,4,5,6,7, GnTV, HERV-E, HERV-K-MEL, KK-LC-1, KM-HN-1, LAGE-1, LRPAP1, LY6K, MAGE-A1, MAGE-A10, MAGE-A12 m, MAGE-A2, MAGE-A3, MAGE-A4, MAGE-A6, MAGE-A9, MAGE-C1, MAGE-C2, mucin, NA88-A, NY-ESO-1 / LAGE-2, NY-ESO-1 / LAGE-2, SAGE, Sp17, SSX-2, SSX-4, TAG-1, TAG-2, TRAG-3, TRP2-INT2, XAGE-1b / GAGED2. In some embodiments, the αDC1 cell maturation cocktail further comprises an inhibitor of tumor growth factor beta (TGF-β) signaling (such as, for example, LY364947, SD208 or SB431542). Some other exemplary inhibitors of TGF-β signaling include but are not limited to tranilast, losartan, glitazones, and imatinib mesylate, pirfenidone, halofuginone, trabedersen (AP 12009), galunisertib (LY2157299), vactosertib (TEW-7197), LSKL, tnhibitor of thrombospondin (TSP-1), cilengitide, M200, NIS793, fresolimumab (GC1008), AVID200, or ABBV-151. In some embodiments, the in vitro or ex vivo-sensitized T cell has an increase in its Th1, cytotoxic T lymphocyte (CTL) and / or NK-like function, compared to an unsensitized T cell. Attorney Docket No: 11390-018WO1 A. Examples The following examples are put forth so as to provide those of ordinary skill in the art with a complete disclosure and description of how the compounds, compositions, articles, devices and / or methods claimed herein are made and evaluated, and are intended to be purely exemplary and are not intended to limit the disclosure. Efforts have been made to ensure accuracy with respect to numbers (e.g., amounts, temperature, etc.), but some errors and deviations should be accounted for. Unless indicated otherwise, parts are parts by weight, temperature is in °C or is at ambient temperature, and pressure is at or near atmospheric. Example 1: Title: Improved Intratumoral DC Therapies: 4x4 DC. Past efforts to enhance and prolong the duration of the Th1- NK- and CTL-activating (and attracting) effector functions, led to the development of several “type-1-polarized” DC populations, induced by viral mimics, activated CD8+ T cells and NK cells, which produce much higher levels of IL-12p70, the factor need for the clinical benefit of DC therapies, and other desirable effector cell-attracting cytokines and chemokines (IL-18, CCL5, CCL19, CXCL10, CXCL11), but lower levels of “suppressor / regulatory” factors, such as CCL22. Such polarized DCs proved superior to multiple forms of non-polarized DCs in induction of antitumor Th1- NK- and CTLs in preclinical in vitro and in vivo models and were shown capable of inducing clinical responses in patients with advanced cancer, however they still undergo eventual (although significantly delayed) “exhaustion”. The goal of the current invention is to manipulate the balance between the duration of DC initial and DC maturation, to simplify the process of generation of DCs for intratumoral administration (and other uses), and achieve the optimal DC numbers, maturation status and production of the desirable factors: IL-12p70 and CTL-, Th1- and NK cell-attracting chemokines: CXCL10 and CCL5. Dendritic cells (DC) and IL-12p70 in cancer immunity. Dendritic cells are key inducers of immunity). DCs activate the lymph node-based naïve and central memory T cells with MHC / peptide complexes (so-called “signal 1”) and costimulatory molecules (“signal 2”) inducing the expansion of T cells and their effector functions (cytokine production, cytotoxicity, migration to sites of inflammation). In addition, DCs can instruct naïve CD4+T cells to differentiate into Th1-, Th2-, or T regulatory- type effector / memory cells (“signal 3), and differentially promote the development of either type-1, cell-mediated immunity, or type-2 humoral responses. Type-1 Th (Th1) T cells, most desirable in cancer, can directly kill tumor cells and provide CD40L-mediated helper signals for CTL development and maintenance, as Attorney Docket No: 11390-018WO1 well as for the optimal NK cell activity. Induction of Th1 cells is promoted by several DC- produced cytokines, particularly by IL-12p70. IL-12p70 also provides essential signals for the activation, effector functions, and survival of NK cells and cytotoxic T lymphocytes. DC-based cancer vaccines. DC-based vaccines have been increasingly applied in the clinical treatment of patients with cancer. Following the initial success of the multi-epitope melanoma trial (Nestle et al 1998; 30% objective clinical responses), DCs have been used successfully to treat patients with melanoma, lymphoma, and renal cell carcinoma, with long-term responses observed in many of them. However, overall clinical response rates and the survival benefit of the early generation DC vaccines were dissapointing, highlighting the need to improve the design of DC-based vaccines, notably the selection of the most appropriate types of DCs and vaccination regimen(s). Fully-mature DCs induced by IL-1β, TNFα, IL-6, and PGE2(Jonuleit et al.1997) have been consistently observed as superior to immature DCs, in their ability to migrate to the vaccine-draining lymph nodes (LN) and to induce higher numbers of cancer-specific specific T cells in vivo. DCs induced by this “complete cytokine mix” are generally considered as the current “gold standard” in DC-based cancer immunotherapy. However, despite their mature status and their ability to induce IFNγ-producing T cells in vivo, the therapeutic efficacy of these cells was disappointing. One potential factor restricting their efficacy may be their relatively low production of IL-12p70. Unfortunately, the PGE2–based maturation cocktail reduces the ability of DCs to produce IL-12p70 and supports the preferential secretion of IL-12-antagonistic p40 homodimer. For this reason, the desirable combination of high immunostimulatory activity and high responsiveness to lymph-node- directing chemokines, with high capacity to produce IL-12p70 has not been attained by DC preparations used in the past clinical trials. Type-1 polarized DC (DC1) are superior inducers of Th1 cells, CTLs, and cytotoxic NK cells. It was observed that DCs matured in the presence of IFN-γ (type-1 polarized DC or DC1) produce up to 100-fold higher levels of IL-12p70 in response to CD40L stimulation, than similarly-mature DCs induced by LPS alone or by the combination of IL-1β and TNFα. Importantly, DC1s are resistant to tumor-associated immunosuppressive factors, and can produce IL-12p70 upon the interaction with CD4+T cells (such as naïve Th cells) that are themselves unable to produce IFNγ. These features suggest that DC1s can be also effective in immunocompromised cancer patients. It has been observed that IFNα and poly-I:C, a synthetic analogue of dsRNA allows for the generation of DC1 in serum-free cultures (αDC1s), paving the way for the clinical application of cancer vaccines based on the paradigm of DC polarization. When compared to the current “gold standard” DCs (matured by IL-1β, TNFα, IL-6, and PGE2), αDC1s (matured in Attorney Docket No: 11390-018WO1 IL1β / TNFα / IFNα / IFNγ / poly-I:C) induce up to 40-fold more CTLs specific for MART-1, gp100-, and tyrosinase, after a single round of in vitro sensitization. They also strongly enhance cytotoxic Th1-type CD4+T cell responses, and the tumoricidal activity of NK cells. Therefore, while the currently-used DC-based vaccines rely on either immature DCs with high ability to produce IL- 12 but low stimulatory / LN-homing capacity, or mature DCs with high stimulatory / LN-homing functions, but reduced ability to produce IL-12, the possibility to generate DC1s allows us for the first time to combine all of these desirable features within a single vaccine preparation. Alpha-type-1-polarized dendritic cells (αDC1s): Clinical activity in patients with recurrent brain cancer and checkpoint-resistant metastatic melanoma. The ability of αDC1s, monocyte-derived DCs matured in the conditions mimicking virally-induced acute inflammation (IL1β / TNFα / IFNα / IFNγ poly-I:C) to selectively induce and amplify CTLs, TH1 and NK cell responses, led to their applications in the therapy of cancer. It was demonstrated that αDC1 loaded with glioma-specific peptide epitopes (IL-13Ra2345-353:1A9V, gp100209-217:2M, EphA2883-891 and YKL-40201-210 ) combined with a TLR3 ligand, poly-ICLC, which induces the intratumoral production of CXCL9, CXCL10, CXCL11 and CCL5 which attract the CXCR3- and CCR5-expressing CTLs and Th1 cells to multiple tumors, including brain tumors, can induce clinical responses and long-term disease stabilizations even in in patients with particularly aggressive recurrent primary brain cancers (high-grade gliomas: AA and GBM (NCT00766753: Fig 1, left; Okada, Kalinski et al.2011). Among the 19 vaccinated patients with recurrent high-grade gliomas (65% GBM, average progression-free survival: 2 months; 35% anaplastic astrocytoma; average progression- free survival: 4 months) they have obseved PFS of at least 12 m in 9 / 19 patients. Even more strikingly 4 (21%) patients developed objective radiologic responses, and two patients (11%) survived at least 5 years. The demonstration that DC1 vaccines loaded with the tumor-relevant peptide antigens can induce long-term stabilizations and objective clinical responses in patients with brain cancer (recurrent GBM), traditionally considered an immuno-privileged site, provides strong evidence for the ability of αDC1 vaccination in BMBC to overcome the immunosuppressive tumor microenvironment in the brain. The most recent trial in metastatic checkpoint-resistant melanoma (NCT01876212) utilizing αDC1s loaded with six antigenic peptides targeting tumor-associated blood vessel antigens (TBVA; uniformly expressed on blood vessels of multiple human and mouse tumors has demonstrated massive epitope spreading and objective radiologic responses in 4 patients (and additional 2 pts with stable disease of at least 9 months), in 12 patients who had previously progressed on PD-1 blockade alone or combined PD-1 / CTLA4 blockade, including 4 objective Attorney Docket No: 11390-018WO1 responses in 7 patients who had previously shown primary PD1-resistance (Fig.1-right, Storkus, Kalinski et al.). These data demonstarte that αDC1 loaded with antigens relevant to different tumors are able to induce effective immunity even against most agressive tumors, such as brain tumors or checkpoint-resistant meatastatic melanoma. Importance of selective induction and attraction of CTLs and Th1 cells, but not Tregs. CTL infiltration of the tumor predicts both improved response to therapy and overall survival. This is true in multiple other tumor types. It also and facilitates responsiveness of multiple cancer types to checkpoint blockers (such as PD1 / PD-L1 / PD-L2 and CTLA4, as well as TIM3 or LAG3) the new class of potent immunotherapeutic agents. In contrast, intratumoral prevalence of regulatory T cells (Tregs) is associated with poor tumor response and impaired survival in patients with many types of cancer. These findings highlight the potential for modulating TIL densities in the management of cancer, by selective induction of CTLs and Th1 cells, rather than Tregs, or their selective attraction. Accordingly, enhanced infiltration of CD8+T cells following modulation of TME can improve spontaneous control of tumor growth and the effectiveness of PD1 and CTLA4 blockade in multiple mouse models. Importantly, for this area of cancer therapies, disclosed herein is that “non-exhausted” aDC1s selectively produce the chemokines which attract the desirable CTL- (both memory- and effector), Th1- and NK cells, as well as other (CCL5, CCL19, CXCL10, CXCL11), as well as factors enhancing their functions, such as IL-12p70 or IL-18, but lower levels of “suppressor / regulatory” factors, such as CCL22, and preferentially attract CTLs, rather than Tregs. DC1s have also been shown to reprogram Th2 cells into Th1 cells and promote enhances attraction and activation of NK cells. αDC1s as modulators of TME and in situ vaccines: Advantages of short-term- activated αDC1s (ST-αDC1s) over αDC1 vaccines and direct injection of DC-activating factors. αDC1s are a specialized type of dendritic cells (DCs), which combine a mature phenotype and high expression of co-stimulatory factors with an elevated, rather than exhausted, ability to produce IL-12p70. In addition to their enhanced ability to cross-present tumor-derived antigens to CD8+T cells recognizing MHC class-I restricted tumor-related antigens in vitro and in vivo, αDC1s effectively convert non-cytolytic CD8+T cells into high perforin- and granzyme B-expressing CXCR3high / CCR5highCTLs, with high killer activity. In phase I / II study in 22 (19 evaluable) patients with recurrent high-grade malignant gliomas (expected time to progression of 2-4 months), who received systemic αDC1 vaccines (loaded with glioma-relevant peptide antigens) and poly-ICLC (to induce intratumoral CXCL10) nine patients achieved TTP >12 Attorney Docket No: 11390-018WO1 months, with two patients achieving complete radiologic responses and two additional patients undergoing partial (and sustained) responses. However, multiple cancers do not have clearly defined tumor rejection antigens, limiting the applicability of antigenic peptides as the source of tumor-relevant antigens. The use of autologous cancer cells as the source of tumor-relevant antigens bypasses this problem (and allows treatment of the roughly 50% of cancer patients in US population who do not express HLA-A2), but autologous tumor-loaded DCs are logistically difficult to prepare and can only be administered 6 weeks or longer after tumor resection (production of the DC vaccine can only start after tumor resection and verification of successful isolation of cancer cells, then the generation and complete sterility testing takes at least 5 weeks). For this reason, they cannot be used at the moment when they are particularly needed, to prevent the early repopulation of the peritoneal cavity with residual cancer cells which evade chemotherapy and surgery. Alternative uses of polarized DC1s activated ex vivo with no antigen loading, to taking up and cross-presenting tumor-derived antigens in vivo and selectively attracting effector CTLs, Th1- and NK cells to tumors. Mature ex vivo antigen-loaded DCs have been traditionally used as “vaccines” to induce tumor-specific T cells in draining lymph nodes. However, this currently dominant paradigm does not take into account that DCs are also essential in the effector phase of immune responses against cancer and other pathogens, with an especially-high level of DC defect observed within the TME itself. In an attempt to develop a new therapeutic intervention enhancing local numbers of tumor-infiltrating effector- and effector memory T cells (critical for long-term outcomes in CRC), a new type of polarized DC1s (ST-αDC1s, activated ex vivo by synergistically-acting mediators of antiviral responses) have been developed, which are specialized in supporting anti-cancer immunity at the tumor sites, by taking up and cross- presenting tumor-derived antigens and selectively attracting effector CTLs, Th1- and NK cells to tumors. Importantly, local administration of ST-αDC1s offers multi-pronged immune-stimulatory action by simultaneously enhancing both induction and effector immunity. Using ST-αDC1s to promote intratumoral accumulation of CTLs and sensitize tumors to anti-PD1 therapy are both novel approaches. It was observed that dendritic cells (DCs) treated for short periods of time ex vivo with alpha-DC1-inducing cytokine cocktails, involving type-1 and type-2 interferons or and interferon and a TLR ligand or alternative inflammatory mediator, produce much higher levels of CTL / Th1 / NK cell-attracting chemokines than TMEs directly exposed to the same chemokine-inducing factors. Attorney Docket No: 11390-018WO1 Moreover, the production of such desirable chemokines by such short-term ex vivo- activated DCs shows resistance to the immunosuppressive microenvironments of cancer, and can function as effective recruiters of CTLs and promoters of intratumoral CTL accumulation in preclinical human and mouse models of cancer. Such new type of DCs (short-term-matured αDC1; ST-αDC1) specialized in producing high levels of CTL-attracting chemokines in the TME and amplifying local antitumor immunity in situ, can be used to induce local immunity and as therapeutic measure, applied alone, or combined with checkpoint blockade, vaccination of adoptive cell therapies (ACT).

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Claims

Attorney Docket Number: 11390-018WO1 CLAIMS What is claimed is 1. A method of making one or more short-term-matured alpha-type 1-dendritic (ST-αDC1) cell(s), comprising a. culturing one or more monocytic cell(s) with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and b. exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand for less than 18 hours.

2. The method of claim 1, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are formulated in a unitary composition.

3. The method of claim 1, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are maintained separately.

4. The method of any one of claims 1-3, wherein the TLR3 ligand is Polyinosinic:polycytidylic acid (poly-I:C) 5. The method of any one of claims 1-4, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml.

6. The method of any one of claims 1-5, wherein the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml.

7. The method of any one of claims 1-6, wherein the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml .Attorney Docket Number: 11390-018WO1 8. The method of any one of claims 1-7, wherein the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml.

9. The method of any one of claims 4-8, wherein the Polyinosinic:polycytidylic acid (poly- I:C) is at a concentration of about 0.2 ng / ml - 200 μg / ml.

10. The method of any one of claims 1-9, wherein the one or more ST-αDC1 cell(s) is loaded with at least one or more antigenic peptides.

11. The method of any one of claims 1-10, wherein the culture is for 4 days.

12. The method of any one of claims 1-11, wherein the exposure is for about 4 hours.

13. The method of any one of claims 1-12, wherein the exposure is for 4 hours.

14. The method of any one of claims 1-13, wherein the one or more ST-αDC1 cell(s) produces at least 50% increased IL-12p70 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L).

15. The method of any one of claims 1-14, wherein the one or more ST-αDC1 cell(s) produces at least 50% increased CXCL10 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L).

16. The method of any one of claims 1-15, wherein the one or more ST-αDC1 cell(s) produces at least 50% decreased Treg chemokine CCL22 compared to an αDCl cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L).

17. The method of any one of claims 1-16, wherein the one or more immature DC cell(s) are further exposed to an inhibitor of tumor growth factor beta (TGF-β) signaling.

18. The method of claim 17, wherein the inhibitor of TGF-β signaling is LY364947, SD208 or SB431542.Attorney Docket Number: 11390-018WO1 19. A method of treating a pre-cancerous or cancerous condition in a subject comprising administering to the subject a therapeutically effective amount of one or more short-term- matured alpha-type 1-dendritic (ST-αDC1) cell(s).

20. The method of claim 19, wherein the one or more ST-αDC1 cell(s) are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail comprising Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and a TLR3 ligand for less than 18 hours, resulting in the one or more ST-αDC1 cell(s).

21. The method of claim 20, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are formulated in a unitary composition.

22. The method of any one of claims 20-21, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are maintained separately.

23. The method of any one of claims 20-22, wherein the TLR3 ligand is Polyinosinic:polycytidylic acid (poly-I:C) 24. The method of any one of claims 20-23, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml.

25. The method of any one of claims 20-24, wherein the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml.

26. The method of any one of claims 20-25, wherein the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml .

27. The method of any one of claims 20-26, wherein the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml.Attorney Docket Number: 11390-018WO1 28. The method of any one of claims 23-27, wherein the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2 ng / ml - 200 μg / ml.

29. The method of any one of claims 20-28, wherein the culture is for 4 days.

30. The method of any one of claims 20-29, wherein the exposure is for about 4 hours.

31. The method of any one of claims 20-30, wherein the exposure is for 4 hours.

32. The method of any one of claims 19-31, wherein one or more ST-αDC1 cell(s) is loaded with at least one or more antigenic peptides.

33. The method of any one of claims 19-32, wherein the one or more ST-αDC1 cell(s) produces at least 50% increased IL-12p70 in a subject compared to a control.

34. The method of any one of claims 19-33, wherein the one or more ST-αDC1 cell(s) produces at least 50% increased CXCL10 compared in a subject compared to a control.

35. The method of any one of claims 19-34, wherein the one or more ST-αDC1 cell(s) produces at least 50% decreased Treg chemokine CCL22 compared in a subject compared to a control.

36. The method of any one of claims 19-35, wherein the one or more ST-αDC1 cell(s) increases intratumoral accumulation of cytotoxic T lymphocytes (CTLs) compared to a control and sensitizes tumors to anti-PD1 therapy.

37. The method of any one of claims 33-36, wherein the control is an untreated subject and / or a subject treated with an αDC1 cell exposed to the αDC1 cell maturation cocktail for 18 hours or more, after 24 hours of stimulation with synthetic CD40 ligand (CD40L).

38. The method of any one of claims 19-37, wherein the one or more ST-αDC1 cell(s) are administered to the subject as a systemic injection.

39. The method of any one of claims 19-38, wherein the one or more ST-αDC1 cell(s) are administered to the subject intratumorally.Attorney Docket Number: 11390-018WO1 40. The method of any one of claims 19-39, wherein the one or more ST-αDC1 cell(s) are administered to the subject within a peritumoral intracavity.

41. The method of any one of claims 20-40, wherein the one or more immature DC cell(s) are further exposed to an inhibitor of tumor growth factor beta (TGF-β) signaling.

42. The method of claim 41, wherein the inhibitor of TGF-β signaling is LY364947, SD208 or SB431542.

43. The method of any one of claims 19-42, further comprising: a. isolating one or more T cells from the subject; b. sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST-αDC1 cell(s) ex vivo; and c. administering to the subject, the one or more ex vivo-sensitized T cell(s).

44. An adoptive cell therapy comprising one or more ST-αDC1 cell(s) and / or one or more in vitro or ex vivo-sensitized T cell(s), wherein the one or more in vitro or ex vivo-sensitized T cell(s) is activated by one or more ST-αDC1 cell(s), wherein the one or more ST-αDC1 cell(s) are made by a method wherein one or more monocytic cell(s) is cultured with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and the one or more immature DC cell(s) is exposed to an αDC1 cell maturation cocktail for less than 18 hours, resulting in the one or more ST-αDC1 cell(s), wherein the αDC1 cell maturation cocktail comprises Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or a TLR-3 ligand.

45. The adoptive cell therapy of claim 44, wherein the TLR3 ligand is Polyinosinic:polycytidylic acid (poly-I:C) 46. The adoptive cell therapy of any one of claims 44-45, wherein the αDC1 cell maturation cocktail comprises Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and Polyinosinic:polycytidylic acid (poly-I:C) are formulated in a unitary composition.Attorney Docket Number: 11390-018WO1 47. The adoptive cell therapy of any one of claims 44-45, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or Polyinosinic:polycytidylic acid (poly-I:C) are maintained separately.

48. The adoptive cell therapy of any one of claims 44-47, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml.

49. The adoptive cell therapy of any one of claims 44-48, wherein the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml.

50. The adoptive cell therapy of any one of claims 44-49, wherein the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml .

51. The adoptive cell therapy of any one of claims 44-50, wherein the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml.

52. The adoptive cell therapy of any one of claims 45-51, wherein the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2 ng / ml - 200 μg / ml.

53. The adoptive cell therapy of any one of claims 44-52, wherein the culture is for 4 days.

54. The adoptive cell therapy of any one of claims 44-53, wherein the exposure is for about 4 hours.

55. The adoptive cell therapy of any one of claims 44-54, wherein the exposure is for 4 hours.

56. The adoptive cell therapy of any one of claims 44-55, wherein the one or more immature DC cell(s) are loaded with at least one or more antigenic peptides.

57. The adoptive cell therapy of any one of claims 44-56, wherein the one or more immature DC cell(s) are further exposed to an inhibitor of tumor growth factor beta (TGF-β) signaling.Attorney Docket Number: 11390-018WO1 58. The adoptive cell therapy of claim 57, wherein the inhibitor of TGF-β signaling is LY364947, SD208 or SB431542.

59. The adoptive cell therapy of any one of claims 44-58, wherein the in vitro or ex vivo- sensitized T cell has an increase in its Th1, cytotoxic T lymphocyte (CTL) and / or NK- like function, compared to an unsensitized T cell.

60. A method of treating a pre-cancerous or cancerous condition in a subject comprising a. isolating one or more T cell(s) from the subject b. sensitizing the one or more T cell(s) by contacting the one or more T cell(s) to one or more ST-αDC1 cell(s) ex vivo, wherein the one or more ex vivo- sensitized T cell(s); and c. administering to a subject in need thereof, the one or more ex vivo-sensitized T cell(s).

61. The method of claim 60, wherein the one or more ST-αDC1 cell(s) are made by a method comprising: a. culturing one or more monocytic cell(s) with GM-CSF, IL-4 or a combination thereof for about 4 days to make one or more immature DC cell(s); and b. exposing the one or more immature DC cell(s) to an αDC1 cell maturation cocktail for less than 18 hours, resulting in the one or more ST-αDC1 cell(s); wherein the αDC1 cell maturation cocktail comprises Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or a TLR3 ligand 62. The method of claim 61, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are formulated in a unitary composition.

63. The method of any one of claims 61-62, wherein the Interleukin 1β (IL1β), Tumor necrosis factor α (TNFα), Interferon α (IFNα), Interferon γ (IFNγ), and / or the TLR3 ligand are maintained separately.

64. The method of any one of claims 61-63, wherein the TLR3 ligand is Polyinosinic:polycytidylic acid (poly-I:C)Attorney Docket Number: 11390-018WO1 65. The method of any one of claims 61-64, wherein the Interleukin 1β (IL1β) is at a concentration of about 0.2-200 ng / ml.

66. The method of any one of claims 61-65, wherein the Tumor necrosis factor α (TNFα) is at a concentration of about 0.2-200 ng / ml.

67. The method of any one of claims 61-66, wherein the Interferon α (IFNα) is at a concentration of about 1-10,000 U / ml .

68. The method of any one of claims 61-67, wherein the Interferon γ (IFNγ) is at a concentration of about 1-10,000 U / ml.

69. The method of any one of claims 64-68, wherein the Polyinosinic:polycytidylic acid (poly-I:C) is at a concentration of about 0.2 ng / ml - 200 μg / ml.

70. The method of any one of claims 61-69, wherein the culture is for 4 days.

71. The method of any one of claims 61-70, wherein the exposure is for about 4 hours.

72. The method of any one of claims 61-71, wherein the exposure is for 4 hours.

73. The method of any one of claims 61-72, wherein the one or more immature DC cell(s) are loaded with at least one or more antigenic peptides.

74. The method of any one of claims 61-73, wherein the one or more immature DC cell(s) are further exposed to an inhibitor of tumor growth factor beta (TGF-β) signaling.

75. The method of claim 74, wherein the inhibitor of TGF-β signaling is LY364947, SD208 or SB431542.

76. The method of any one of claims 60-75, wherein the one or more ex vivo-sensitized T cell(s) has an increase in its Th1, cytotoxic T lymphocyte (CTL) and / or NK-like function, compared to an unsensitized T cell.

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