T Cells Engineered to Express Interleukin 7 and C-C motif Chemokine Ligand 19 Field The present invention relates to the modification of T cells to increase their cytotoxic activity and the use of modified T cells in immunotherapy, for example for the treatment of solid cancers. Background T cells (or T lymphocytes) are found widely distributed within tissues and the tumour environment. T cells are distinguished from other lymphocytes by the presence of T cell receptors (TCRs) on the cell surface. The TCR is a multi-subunit transmembrane complex that mediates the antigen-specific activation of T cells. The TCR confers antigen specificity on the T cell, by recognising an antigen peptide ligand that is presented on the target cell by a major histocompatibility complex (MHC) molecule. Although peptides derived from altered or mutated proteins in tumour target cells can be recognised as foreign by T cells expressing specific TCRs, many antigens on tumour cells are simply upregulated or overexpressed (so called self-antigens) and do not induce a functional T cell response. Therefore, studies have focussed on identifying target tumour antigens which are expressed, or highly expressed, in the malignant but not the normal cell type. Examples of such targets include the cancer/testis (CT) antigen NY-ESO-1, which is expressed in a wide array of human cancers but shows restricted expression in normal tissues (Chen Y-T et al. Proc Natl. Acad. Sci USA.1997; 94(5):1914-1918), and the MAGE- A family of CT antigens which are expressed in a very limited number of healthy tissues (Scanlan M. J. et al. Immunol Rev.2002; 188:22–32). Identification of such antigens has promoted the development of targeted T cell-based immunotherapy, which has the potential to provide specific and effective cancer therapy (Ho, W.Y. et al. Cancer Cell 2003; 3:1318-1328; Morris, E.C. et al. Clin. Exp. Immunol.2003; 131:1-7; Rosenberg, S.A. Nature 2001; 411:380-384; Boon, T. and van der Bruggen P. J. Exp. Med.1996; 183:725-729). The intravenous administration of interleukin 7 (IL-7) has been proposed to improve outcomes in T cell-based immunotherapy. IL-7 is known to bolster the persistence of tumour- specific T-cells (Melchionda, F. et al. J. Clin. Invest.2005;115:1177-87), and T-cells genetically modified to either secrete IL-7 or overexpress the IL-7 receptor (in conjunction with administered IL-7) display enhanced antitumour efficacy in preclinical models (Vera, J.F. et al. Mol. Ther.2009;17:880-8, Markley, J.C. and Sadelain, M. Blood 2010;115:3508- 3519). However, systemic administration of cytokines to patients with cancer has caused significant toxicity (Sportes, C. et al. Clin. Cancer Res.2010; 16:727-35, Conlon, K.C. t al. J. Clin. Oncol.2015;33:74-82, Brudno, J.N. et al. Blood 2016;127:3321-31). Alternative approaches such as genetic modification of T-cells to secrete or trans-present cytokines (Hutton L.V. et al. Proc. Natl. Acad. Sci. USA 2016;113:E7788-97) carry a risk of severe adverse events, including neurotoxicity and cytokine release syndrome from systemic accumulation of secreted cytokine (Zhang, L. et al. Clin. Cancer Res.21; 21:2278-88), whereas T-cells that overexpress cytokine receptors do not eliminate the need for exogenous cytokine (Vera, J.F. et al. Mol. Ther.2009; 17:880-8). The generation of immunocompetent cells that express IL-7, CCL19 and a cell surface molecule that specifically recognizes a cancer antigen has been reported (EP3431597A1). In addition, the administration of T cells expressing IL-7, CCL19 and a chimeric antigen receptor (CAR) has been found to induce a memory function in endogenous T cells (EP3695846A1). The expression of IL-7 and CCL19 in CAR-T cells has also been reported to improve the infiltration and survival of CAR-T cells (Adachi et al Nature Biotech (2018) 36 4346-351; Duan D, et al. Front Immunol.2021; 12:609421; Goto S, et al. Cancer Immunol Immunother.2021;70:2503-2515; Pang et al (2021) J. Hematol. Oncol.14118) and to enhance the anti-tumour responses of TCR-T cells (Tokunaga Y et al. (2021) Mol Cancer Ther.2021. doi: 10.1158/1535-7163). Summary The present inventors have recognised that the expression of interleukin 7 (IL-7) and C-C motif chemokine ligand 19 (CCL19) unexpectedly improves the anti-tumour properties of T cells expressing a heterologous T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4. A first aspect of the invention provides a T cell that expresses a heterologous T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4 and further expresses heterologous interleukin 7 (IL-7) and heterologous C-C motif chemokine ligand 19 (CCL19). A T cell of the first aspect may comprise; (i) a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4; (ii) a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19); and (iii) a third heterologous nucleotide sequence encoding interleukin 7 (IL-7). A second aspect of the invention provides a nucleic acid construct comprising; (i) a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4; (ii) a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19); and (iii) a third heterologous nucleotide sequence encoding interleukin 7 (IL-7). Preferred TCRs of the first and second aspect are human affinity enhanced TCRs. A third aspect of the invention provides a vector, for example a lentiviral vector, comprising a nucleic acid construct of the second aspect. A fourth aspect of the invention provides a population of T cells according to the first aspect. A fifth aspect of the invention provides a pharmaceutical composition comprising a population of T cells according to the fourth aspect and a pharmaceutically acceptable excipient. A sixth aspect of the invention provides a population of T cells according to the fourth aspect for use in a method of treatment of the human or animal body, for example a method of treatment of cancer in an individual. Related aspects provide the use of a population of T cells according to the fourth aspect in the manufacture of a medicament for the treatment of cancer in an individual and a method of treating cancer comprising administering to an individual with cancer a population of T cells according to the fourth aspect. A seventh aspect of the invention provides a method of producing a population of modified T cells comprising; introducing a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4; a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19); and a third heterologous nucleotide sequence encoding interleukin 7 (IL-7) into a population of T cells obtained from a donor individual to produce a population of modified T cells. A method of the seventh aspect may comprise introducing a nucleic acid construct or a vector according to the second or third aspects into a population of T cells obtained from a donor individual to produce a population of modified T cells. An eighth aspect of the invention provides a method of producing a population of modified T cells comprising; introducing a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4; a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19); and a third heterologous nucleotide sequence encoding interleukin 7 (IL-7) into a population of progenitor cells; and differentiating the population of progenitor cells into a population of modified T cells. A method of the eighth aspect may comprise introducing a nucleic acid construct or a vector according to the second or third aspects into the population of progenitor cells. Progenitor cells for use in methods of the eighth aspect may include induced pluripotent stem cells (iPSCs), mesoderm cells (MCs), haematopoietic progenitor cells (HPCs) or progenitor T cells. Populations of modified T cells produced by a method of the seventh or eighth aspect may include a population of T cells of the fourth aspect. A ninth aspect of the invention provides a method of treating cancer in an individual in need thereof comprising; producing a population of modified T cells by a method of the seventh or eighth aspect, and administering the population of modified T cells to a recipient individual. A tenth aspect of the invention provides a method of treating cancer in an individual in need thereof comprising; introducing a nucleic acid construct or a vector according to the second or third aspects into a population of T cells obtained from a donor individual to produce a population of modified T cells, and administering the population of modified T cells to a recipient individual. The donor individual and the recipient individual may be the same (i.e. autologous treatment; the modified T cells are obtained from an individual who is subsequently treated with the modified T cells) or the donor individual and the recipient individual may be different (i.e. allogeneic treatment; the modified T cells are obtained from one individual and subsequently used to treat a different individual). Suitable cancers for treatment in accordance with the ninth or tenth aspects include solid tumours. Other aspects and embodiments of the invention are described below. Brief Description of Figures Figure 1 shows the change in T-cell counts following antigen stimulation. ADP-A2M4, ADP- A2M4N7X19 and ntd (non-transduced) T-cells from 3 donors were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells. Cell counts were performed every 7-days and used to calculate fold-change from the known density of cells seeded. Figure 2 shows the change in CD8 and TCR-positive and TCR-negative fractions of ADP-A2M4N7X19 following antigen stimulation. ADP-A2M4N7X19 were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells. In figure 2A, CD8 and anti-TCR antibodies were used to determine all possible combinations of expression patterns for the two markers on CD45+ T-cells. Each subset frequency was calculated by multiplying TCR+/- frequency with the parental CD8+/- frequency. The sum of these was assumed to be 100 % and each frequency was expressed as a percentage of this (normalized frequency). In figure 2B, absolute cell counts were performed every 7 days (CD45+ T-cells/mL) and used to calculate fold change from the known density of cells seeded (0.5 x 106 CD45+ T-cells/mL). The frequency data (from section A) was then applied to these counts to calculate fold-change from day 0. Solid and dashed lines indicate CD8+ and CD8- populations. Figure 3 shows cell counting safety. ADP-A2M4, ADP-A2M4N7X19, and non-transduced (ntd) cells from 2 donors were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells in the absence or presence of 20 ng/mL exogenous rhIL-7 (top and bottom panels, respectively). On day 7 (vertical dashed line) antigen was removed (dotted lines). Absolute cell counts were performed every 7 days (CD45 ⁺ T-cells/mL) and used to calculate fold-change from the known density of cells seeded. Figure 4 shows IFNγ production. ADP-A2M4, ADP-A2M4N7X19 and ntd (non-transduced) T- cells from 3 donors were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells. Supernatants were collected at day 1, 7, 8, 14, 15, 21, 22, and 28 and cytokine levels (pg/mL) determined on supernatants. Each point represents the mean from duplicate wells from a single condition. Closed circles represent points falling within the range of the standard curve. Open circles represent data above or below the range of the standard curve. Figure 5 shows IL-7 production. ADP-A2M4, ADP-A2M4N7X19 and ntd (non-transduced) T- cells from 3 donors were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells. Supernatants were collected at day 1, 7, 8, 14, 15, 21, 22, and 28 and cytokine levels (pg/mL) determined on supernatants. Each point represents the mean from duplicate wells from a single condition. Closed circles represent points falling within the range of the standard curve. Open circles represent data above or below the range of the standard curve. Figure 6 shows CCL19 production. ADP-A2M4, ADP-A2M4N7X19 and ntd (non-transduced) T-cells from 3 donors were stimulated on a weekly basis with irradiated A375 (MAGE-A4 antigen-positive) cells. Supernatants were collected at day 1, 7, 8, 14, 15, 21, 22, and 28 and cytokine levels (pg/mL) determined on supernatants. Each point represents the mean from duplicate wells from a single condition. Closed circles represent points falling within the range of the standard curve. Open circles represent data above or below the range of the standard curve. Figure 7 shows mDC migration towards activated ADP-A2M4N7X19. ADP-A2M4, ADP- A2M4N7X19, ADP-A2M4IL7 and ntd (non-transduced) T-cells from 3 donors were incubated with NCI-H1755 (MAGE-A4 antigen-positive) cells in the lower chamber of a transwell plate for 48 hours. The upper chamber, pre-seeded with primary dermal microvascular endothelial cells, had fluorescently stained mDCs added followed by measurement of migration in a plate reader over 6 hours. A positive control of rh-CCL19 was added to independent wells. Figure 8 shows the cytotoxic activity of ADP-A2M4N7X19 in response to tumor cell lines. The tumor target cell lines, A375 (HLA-A2+/MAGE-A4 ⁺ ), and Colo205 (HLA-A2 ⁺ /MAGE-A4-) were cultured in the absence or presence of MAGE-A4 peptide (10 ^-6 and 10 ^-8 M), were co- incubated with afamitresgene autoleucel (red), ADP-A2M4N7X19 (blue) or ntd (non- transduced; grey) from 3 donors (Wave266, Wave267 and Wave268). Wells containing targets cells only (black) were a control for background target cell death. IncuCyte® Caspase-3/7 Green Dye reagent was added to all the wells, followed by peptide to the relevant wells. A single image was taken of each well every 3h for a period of 72h. The number of green (caspase3/7 ⁺ ) objects/mm ² , a measure of target cells undergoing apoptosis, was determined and plotted against time. Data shows mean +/- SEM of triplicate wells. Figure 9 shows the survival rate of P1A-TCR in vivo study. Vehicle = Group 1; P1A- TCR_eGFP = Group 2; P1A-TCR_7X19_eGFP = Group 3; P1A-TCR_eGFP_inducibleIL- 7_constitutiveCCL19 = Group 4; P1A-TCR_eGFP_inducibleIL-7_inducibleCCL19 = Group 5. * p<0.05. ** p<0.01: Significantly different from the vehicle group by log-rank test. Figure 10 shows CCL19 (top) and IL-7 (bottom) production by T-cells transfected with different constructs and stimulated with different MAGE-A4 antigen-positive cells. Detailed Description This invention relates to T cells that express a heterologous T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4. The T cells are further modified to express heterologous interleukin 7 (IL-7) and heterologous C-C motif chemokine ligand 19 (CCL19). The expression of IL-7 and CCL19 is shown herein to improve the anti-tumour activity of the T cells described herein. For example, the T cells may show improved or enhanced survival and proliferation and/or reduced T-cell exhaustion relative to T cells that do not express IL-7 and CCL19. Alternatively, or additionally, the T cells may increase the survival and proliferation of other immune cells, such as tumour infiltrating lymphocytes (TILs), in the tumour microenvironment of a patient, for example through paracrine effects; and/or the T cells may increase and/or accelerate the migration of other immune cells, such as dendritic cells (DCs), into the solid tumour of a patient. These effects may improve or enhance the anti-tumour effect of the T cells relative to T cells that do not express heterologous IL-7 and CCL19. For example, T cells described herein stimulated on a weekly basis with irradiated MAGE-A4 antigen-positive cells as described herein may secrete 10-fold or more, 20-fold or more, 30- fold or more, 50-fold or more or 100-fold or more IFNγ at day 22 relative to T cells that do not express heterologous IL-7 and CCL19. T cells described herein that are stimulated on a weekly basis with irradiated MAGE-A4 antigen-positive cells as described herein may show an increase in cell count of 10-fold or more, 20-fold or more, 30-fold or more, 50-fold or more or 100-fold or more at day 28 relative to T cells that do not express heterologous IL-7 and CCL19. T cells as described herein that are stimulated with MAGE-A4 antigen-positive cells. for example in a transwell assay described herein may increase the migration of dendritic cells by 2-fold or more, 3-fold or more, or 4-fold or more after 6 hours relative to T cells that do not express heterologous IL-7 and CCL19. T cells (also called T lymphocytes) are white blood cells that play a central role in cell- mediated immunity. T cells can be distinguished from other lymphocytes by the presence of a T cell receptor (TCR) on the cell surface. T-cells do not express endogenous IL-7 or CCL19. There are several types of T cells, each type having a distinct function. T helper cells (T _H cells) are known as CD4 ⁺ T cells because they express the CD4 surface glycoprotein. CD4 ⁺ T cells play an important role in the adaptive immune system and help the activity of other immune cells by releasing T cell cytokines and helping to suppress or regulate immune responses. They are essential for the activation and growth of cytotoxic T cells. Cytotoxic T cells (TC cells, CTLs, killer T cells) are known as CD8 ⁺ T cells because they express the CD8 surface glycoprotein. CD8 ⁺ T cells act to destroy virus-infected cells and tumour cells. Most CD8 ⁺ T cells express TCRs that can recognise a specific antigen displayed on the surface of infected or damaged cells by a class I MHC molecule. Specific binding of the TCR and CD8 glycoprotein to the antigen and MHC molecule leads to T cell- mediated destruction of the infected or damaged cells. T cells for use as described herein may be CD4 ⁺ T cells; CD8 ⁺ T cells; or CD4 ⁺ T cells and CD8 ⁺ T cells. In some preferred embodiments, the T cells may be a mixed population of CD4 ⁺ T cells and CD8 ⁺ T cells. Suitable T cells for use as described herein are human T cells and may be obtained, for example from a donor individual. In some preferred embodiments, the donor individual may be the same person as the recipient individual to whom the T cells will be administered following modification and expansion as described herein (autologous treatment). In other embodiments, the donor individual may be a different person to the recipient individual to whom the T cells will be administered following modification and expansion as described herein (allogeneic treatment). For example, the donor individual may be a healthy individual who is human leukocyte antigen (HLA) matched (either before or after donation) with a recipient individual suffering from cancer. Other suitable T cells may be obtained by the directed differentiation or forward programming of pluripotent stem cells, such as induced pluripotent stem cells (iPSCs). Suitable methods are described in for example WO2021/032855, WO2021/032851, WO2021/032852 and WO2021/032836. A method described herein may comprise the step of obtaining T cells from a donor individual and/or isolating T cells from a sample obtained from a donor individual with cancer. A population of T cells may be isolated from a blood sample. Suitable methods for the isolation of T cells are well known in the art and include, for example fluorescent activated cell sorting (FACS: see for example, Rheinherz et al (1979) PNAS 764061), cell panning (see for example, Lum et al (1982) Cell Immunol 72122) and isolation using antibody coated magnetic beads (see, for example, Gaudernack et al 1986 J Immunol Methods 90179). CD4 ⁺ and CD8 ⁺ T cells may be isolated from the population of peripheral blood mononuclear cells (PBMCs) obtained from a blood sample. PBMCs may be extracted from a blood sample using standard techniques. For example, ficoll ^TM may be used in combination with gradient centrifugation (Böyum A. Scand J Clin Lab Invest.1968; 21(Suppl.97):77-89), to separate whole blood into a top layer of plasma, followed by a layer of PBMCs and a bottom fraction of polymorphonuclear cells and erythrocytes. In some embodiments, the PBMCs may be depleted of CD14 ⁺ cells (monocytes). Following isolation, the T cells may be activated. Suitable methods for activating T cells are well known in the art. For example, the isolated T cells may be exposed to a T cell receptor (TCR) agonist. Suitable TCR agonists include ligands, such as a peptide displayed on a class I or II MHC molecule on the surface of an antigen presenting cell, such as a dendritic cell, and soluble factors, such as anti-TCR antibodies. An anti-TCR antibody may specifically bind to a component of the TCR, such as εCD3, αCD3 or αCD28. Anti-TCR antibodies suitable for TCR stimulation are well-known in the art (e.g. OKT3) and available from commercial suppliers (e.g. eBioscience CO USA). In some embodiments, T cells may be activated by exposure to anti-αCD3 antibodies and IL2. More preferably, T cells are activated by exposure to anti-αCD3 antibodies and anti-αCD28 antibodies. The activation may occur in the presence or absence of CD14 ⁺ monocytes. Preferably, the T cells may be activated with anti-CD3 and anti-CD28 antibody coated beads. For example, PBMCs or T cell subsets including CD4 ⁺ and/or CD8 ⁺ cells may be activated, without feeder cells (antigen presenting cells) or antigen, using antibody coated beads, for example magnetic beads coated with anti-CD3 and anti-CD28 antibodies, such as Dynabeads® Human T-Activator CD3/CD28 (ThermoFisher Scientific). T cells described herein express heterologous IL-7 and CCL19 in addition to a heterologous TCR that specifically binds to cancer cells that express MAGE A4. Interleukin 7 (IL-7) is a haematopoietic cytokine that binds to the heterodimeric IL-7 receptor and is involved in T lymphopoiesis in the thymus, T-cell homeostasis, lymphopenia-driven proliferation and regulation of lymph node organogenesis. IL-7 may be human IL-7 (Gene ID 3574) and may have the reference amino acid sequence of NP_00871.1 (SEQ ID NO: 2 or SEQ ID NO: 4) and may be encoded by the reference nucleotide sequence of NM_000880.4 (SEQ ID NO: 1). In some preferred embodiments, a nucleotide sequence encoding IL-7 may be codon-optimised for expression in human T cells. For example, nucleotide sequence encoding IL-7 may have the nucleotide sequence of SEQ ID NO: 3. C-C motif chemokine ligand 19 (CCL19) is a cytokine that binds to the chemokine receptor CCR7 and acts on migratory cells of the adaptive immune system, including naïve T-cells, central memory T-cells, regulatory T-cells, naïve B-cells, semi-mature/mature dendritic cells (DCs) and natural killer (NK) cells. CCL19 may be human CCL19 (Gene ID 6363) and may have the reference amino acid sequence of NP_006265.1 (SEQ ID NO: 7) and may be encoded by the reference nucleotide sequence of NM_006274.3 (SEQ ID NO: 5; coding sequence residues 138-434). In some preferred embodiments, a nucleotide sequence encoding CCL19 may be codon optimised for expression in human T cells. For example, nucleotide sequence encoding CCL19 may have the nucleotide sequence of SEQ ID NO: 6. T cell receptor (TCRs) are disulphide-linked membrane anchored heterodimeric proteins, typically comprising highly variable alpha (α) and beta (β) chains expressed as a complex with invariant CD3 chain molecules. T cells expressing this type of TCR are commonly referred to as α:β (or αβ) T cells. A minority of T cells express an alternative TCR comprising variable gamma (γ) and delta (δ) chains and are referred to as γδ T cells. The T cells described herein express a heterologous T cell receptor (TCR) that binds to cancer cells expressing melanoma-associated antigen A4 (MAGE-A4). Suitable TCRs bind specifically to a major histocompatibility complex (MHC) on the surface of cancer cells that displays a peptide fragment of the tumour antigen MAGE A4. For example, the T cells may be modified to express a heterologous TCR that binds specifically to MHCs displaying peptide fragments of the tumour antigen MAGE A4 that are expressed by the cancer cells in a specific cancer patient. The expression of MAGE A4 by cancer cells in the cancer patient may identified using standard techniques. A heterologous TCR may be a synthetic or artificial TCR i.e. a TCR that does not exist in nature. For example, a heterologous TCR may be engineered to increase its affinity or avidity for a tumour antigen (i.e. an affinity enhanced TCR). The affinity enhanced TCR may comprise one or more mutations relative to a naturally occurring TCR, for example, one or more mutations in the hypervariable complementarity determining regions (CDRs) of the variable regions of the TCR α and β chains. These mutations alter the affinity of the TCR for MHCs that display a peptide fragment of the tumour antigen MAGE A4 expressed by cancer cells, such that the affinity is sufficient for activity without cross-reactivity. For example, a TCR bind to an MHC displaying a peptide fragment of the tumour antigen MAGE A4 with a dissociation constant of 0.05μΜ to 20.0μΜ; for example, 0.1μΜ to 5μΜ or 0.2μΜ to 2μΜ. Suitable methods of generated affinity enhanced TCRs include screening libraries of TCR mutants using phage or yeast display; and measuring binding affinity are well known in the art (see for example Robbins et al J Immunol (2008) 180(9):6116; San Miguel et al (2015) Cancer Cell 28 (3) 281-283; Schmitt et al (2013) Blood 122348-256; Jiang et al (2015) Cancer Discovery 5901). TCRs for use as described herein bind to cancer cells that express MAGE A4. Expression of the heterologous TCR may alter the immunogenic specificity of the T cells so that they recognise or display improved recognition for one or more MAGE A4 derived tumour antigens that are present on the surface of the cancer cells of an individual with cancer. In some embodiments, the T cells may display reduced binding or no binding to cancer cells that express MAGE A4 in the absence of the heterologous TCR. For example, expression of the heterologous TCR may increase the affinity and/or specificity of the cancer cell binding of modified T cells relative to unmodified T cells. MAGE A4 is a highly immunogenic member of the MAGE-A family of Cancer/Testis (CT) antigens and is expressed in testes and placenta but not in other types of healthy tissue. MAGE A4 is expressed in high percentages of cancer cells from a number of tumours, including melanoma, head and neck squamous cell carcinoma, lung carcinoma and breast carcinoma. Melanoma-associated antigen A4 (MAGE-A4) may be human MAGE A4 (Gene ID 4103) and may have the reference amino acid sequence of NP_001011548.1 (SEQ ID NO: 9) and may be encoded by the reference nucleotide sequence of NM_000880.4 (SEQ ID NO: 8). An MHC is a set of cell-surface proteins which allow the acquired immune system to recognise ‘foreign’ molecules. Proteins are intracellularly degraded and presented on the surface of cells by the MHC. MHCs displaying ‘foreign’ peptides, such a viral or cancer associated peptides, are recognised by T cells with the appropriate TCRs, prompting cell destruction pathways. MHCs on the surface of cancer cells may display peptide fragments of tumour antigen i.e. an antigen which is present on a cancer cell but not the corresponding non-cancerous cell. T cells which recognise these peptide fragments may exert a cytotoxic effect on the cancer cell. TCRs for use as described herein bind to a peptide fragment of MAGE A4. In some preferred embodiments, the peptide fragment of MAGE-A4 is GVYDGREHTV (residues 230- 239 of MAGE-A4; SEQ ID NO: 10). In some preferred embodiments, the MHC is HLA-A*-201. For example, the peptide fragment of MAGE A4 may be HLA-A*-201 restricted. A preferred TCR may specifically bind to HLA-A*-201 complexed with the MAGE A4 peptide GVYDGREHTV. For example, a TCR binds to GVYDGREHTV (SEQ ID NO: 10) in complex with HLA-A* 0201 with a dissociation constant of 0.05μΜ to 20.0μΜ. Dissociation may be measured using surface plasmon resonance at 25 ^o C and at a pH between 7.1 and 7.5 using a soluble form of the TCR. In some embodiments, the TCR may bind to an MHC displaying GVYDGREHTV (SEQ ID NO: 10) preferentially to an MHC displaying the MAGE-B2231240 GVYDGEEHSV (SEQ ID NO: 11) or may bind to an MHC displaying GVYDGREHTV but not to an MHC displaying the MAGE-B2231240 GVYDGEEHSV. For example, the TCR may bind to GVYDGEEHSV (SEQ ID NO: 11) in complex with HLA-A* 0201 with a dissociation constant of 30μΜ to 60μΜ when measured with surface plasmon resonance at 25 ^o C and at a pH between 7.1 and 7.5 using a soluble form of the TCR. In some embodiments, the dissociation constant may be above 50μΜ, such as 100μΜ or more, 200μΜ or more, or 500μΜ or more. In some embodiments, the TCR may comprise a TCR alpha chain variable domain and a TCR beta chain variable domain. The TCR variable domains may form contacts with at least residues V2, Y3 and D4 of GVYDGREHTV (SEQ ID NO: 10). The alpha chain variable domain of the TCR may comprise the amino acid sequence of residues 1 to 111 of SEQ ID NO: 12; SEQ ID NO: 14 or a variant thereof. More preferably, the alpha chain variable domain of the TCR may comprise the amino acid sequence of SEQ ID NO: 14, or residues 22 to 125 of SEQ ID NO: 16 or a variant of either of these. The beta chain variable domain may comprise the amino acid sequence of residues 1 to 111 of SEQ ID NO: 13 a variant thereof. More preferably, the beta chain variable domain of the TCR may comprise the amino acid sequence of SEQ ID NO: 15 or residues 22 to 123 of SEQ ID NO: 17 or a variant of either of these. . In some embodiments, the TCR may comprise the TCR alpha chain amino acid sequence of of residues 22 to 276 of SEQ ID NO: 16 or a variant thereof and the TCR beta chain amino acid sequence of residues 22 to 311 of SEQ ID NO: 17 or a variant thereof. In other embodiments, the TCR may comprise the TCR alpha chain amino acid sequence (residues 22 to 125) and the TCR beta chain amino acid sequence (residues 327 to 624) shown in SEQ ID NO: 18. The alpha and beta chain sequences may be separated by a self-cleaving peptide. This allows the chains of the TCR to be expressed as a single transcript which undergoes ribosomal skipping during translation to generate the two separate proteins. Suitable self- cleaving peptides are well-known in the art and include 2A peptides, such as T2A, P2A, E2A and F2A.2A peptides include the P2A sequence of residues 284-305 of SEQ ID NO: 25. For example, the TCR may comprise the amino acid sequence shown in residues 22 to 617 of SEQ ID NO: 18. A suitable TCR may be encoded by the nucleotide sequence of SEQ ID NO: 19. Suitable TCRs for use as described herein are disclosed in WO2017/174824 and Sanderson et al. Oncoimmunol. (2019) 9 (1):e1682381, the contents of which are incorporated herein by reference. The IL-7, CCL19 and TCR expressed in the modified T cell are recombinant proteins that are encoded by heterologous nucleic acid i.e. the IL-7, CCL19 and TCR are expressed from encoding nucleic acid that has been incorporated into the T cell by recombinant techniques. For example, a T cell described herein may comprise; (i) a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4, (ii) a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19); and (iii) a third heterologous nucleotide sequence encoding interleukin 7 (IL-7). Modification of a T cell to express the IL-7, CCL19 and TCR may comprise introducing the first, second and third nucleotide sequences into the T cell. Suitable methods for the introduction and expression of heterologous nucleic acids into T cells are well-known in the art and described in more detail below. In some embodiments, the T cells may be modified to incorporate the first, second and third nucleotide sequences following isolation and activation. In other embodiments, progenitor cells such as pluripotent stem cells, may be modified to incorporate the first, second and third nucleotide sequences and then differentiated or forward programmed into T cells. In preferred embodiments, the first, second and third nucleotide sequences may be contained in a single nucleic acid construct that is introduced into the T cell or progenitor cell. In some embodiments, the first, second and third nucleotide sequences encoding IL-7, CCL19 and TCR respectively may be contained in a single nucleic acid construct and expressed from a single promoter (i.e. as a single transcript). Preferably, the first, second and third heterologous nucleotide sequences are arranged sequentially in the construct. For example, first nucleotide sequence (i) may be located adjacent the promoter, followed by the second nucleotide sequence (ii) and then the third nucleotide sequence (iii). The first, second and third nucleotide sequences may be separated by nucleotide sequences encoding self-cleaving peptides. This allows the generation of separate proteins from a single transcript by ribosomal skipping during translation. For example, a T cell may comprise; (iv) a fourth nucleotide sequence encoding a self-cleaving peptide, said fourth sequence being located between the first and second nucleotide sequences; and (v) a fifth nucleotide sequence encoding a self-cleaving peptide, said fifth sequence being located between the second and third nucleotide sequences. A suitable construct comprising the first to the fifth nucleotide sequences is shown in SEQ ID NO: 24. Suitable self-cleaving peptides are well-known in the art and include 2A peptides, such as T2A, P2A, E2A and F2A. In some embodiments, the fourth nucleotide sequence may encode a T2A peptide and the fifth nucleotide sequence may encode a F2A peptide. The first to the fifth nucleotide sequences may be operably linked to a single promoter. The promoter may be an inducible promoter or more preferably a constitutive promoter. Suitable constitutive promoters are well known in the art and include mammalian promoters, such as Human elongation factor-1 alpha (EF1α). Expression of the heterologous nucleotide sequence from the constitutive promoter is shown herein to be increased in the T cells following stimulation with antigen. For example, minimal IL-7 and CCL19 may be produced when the cells are in a resting state, but the levels of both may increase to measurable levels upon T cell activation. Suitable inducible promoters may comprise a nuclear factor of activated T cells (NFAT)/AP1 transcriptional response element (TRE). Upon recognition of the cognate peptide MHC1 complex, NFAT undergoes Ca2+ dependent translocation to the nucleus where it promotes transcription of genes which harbour an NFAT TRE. Suitable NFAT TREs are well-known in the art and include the human IL2 promoter NFAT TRE (Macian et al (2001) Oncogene.2001 Apr 30; 20(19):2476-89) which has the sequence of SEQ ID NO: 20 or a variant thereof. The inducible promoter may comprise one, two, three or more repeats of the NFAT TRE. The inducible promoter may further comprise additional promoter elements, for example a minimal viral promoter such as CMV. Suitable promoter elements are well known in the art and include the minimal CMV promoter of SEQ ID NO: 21 or a variant thereof. A suitable inducible promoter sequence operably linked to a nucleotide sequence encoding IL-7 may comprise the nucleotide sequence of SEQ ID NO: 22, SEQ ID NO: 23 or a variant thereof In other embodiments, a T cell may inducibly express IL-7 and/or CCL19. For example, the second nucleotide sequence encoding CCL19 and the third nucleotide sequence encoding IL-7 may be operably linked to inducible promoters. The nucleotide sequences may be operably linked the same or different inducible promoters. Expression of IL-7 and CCL19 from the inducible promoter(s) may be induced by T-cell activation. The first nucleotide sequence encoding the TCR may be constitutively expressed from a constitutive promoter. In some embodiments, the coding sequences for the individual chains of the TCR (e.g. TCRα and TCRβ chains) may be separated by a sequence encoding a self-cleaving peptide. This allows the chains of the TCR to be expressed as a single transcript which undergoes ribosomal skipping during translation to generate the two separate proteins. Suitable cleavage recognition sequences are well known in the art and include 2A-furin sequence. The term “heterologous” refers to a polypeptide or nucleic acid that is foreign to a particular biological system, such as a host cell, and is not naturally present in that system. A heterologous polypeptide or nucleic acid may be introduced to a biological system by artificial means, for example using recombinant techniques. For example, heterologous nucleic acid encoding a polypeptide may be inserted into a suitable expression construct which is in turn used to transform a host cell to produce the polypeptide. A heterologous polypeptide or nucleic acid may be synthetic or artificial or may exist in a different biological system, such as a different species or cell type. An endogenous polypeptide or nucleic acid is native to a particular biological system, such as a host cell, and is naturally present in that system. A recombinant polypeptide is expressed from heterologous nucleic acid that has been introduced into a cell by artificial means, for example using recombinant techniques. A recombinant polypeptide may be identical to a polypeptide that is naturally present in the cell or may be different from the polypeptides that are naturally present in that cell. A variant of a reference amino acid or nucleotide sequence set out herein may comprise a sequence having at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95%, or at least 98% sequence identity to the reference sequence. Particular amino acid sequence variants may differ from a repeat domain shown above by insertion, addition, substitution or deletion of 1 amino acid, 2, 3, 4, 5, 6, 7, 8, 9, or 10 or more than 10 amino acids. Particular nucleotide sequence variants may differ from a reference sequence set out herein by insertion, addition, substitution or deletion of 1 amino acid, 2, 3, 4, 5, 6, 7, 8, 9, or 10 or more than 10 amino acids. Sequence similarity and identity are commonly defined with reference to the algorithm GAP (Wisconsin Package, Accelerys, San Diego USA). GAP uses the Needleman and Wunsch algorithm to align two complete sequences that maximizes the number of matches and minimizes the number of gaps. Generally, default parameters are used, with a gap creation penalty = 12 and gap extension penalty = 4. Use of GAP may be preferred but other algorithms may be used, e.g. BLAST (which uses the method of Altschul et al. (1990) J. Mol. Biol.215: 405-410), FASTA (which uses the method of Pearson and Lipman (1988) PNAS USA 85: 2444-2448), or the Smith-Waterman algorithm (Smith and Waterman (1981) J. Mol Biol.147: 195-197), or the TBLASTN program, of Altschul et al. (1990) supra, generally employing default parameters. In particular, the psi-Blast algorithm (Nucl. Acids Res. (1997) 253389-3402) may be used. Sequence comparison may be made over the full-length of the relevant sequence described herein. The introduction of the heterologous nucleic acid sequences into T cells or progenitor cells and the subsequent expansion of the T cells or progenitor cells may be performed in vitro and/or ex vivo. The first, second and third nucleotide sequences encoding TCR, CCL19 and IL-7, respectively, may be introduced into the T cells or progenitors thereof separately or more preferably in the same nucleic acid construct. This may increase the proportion of T cells or progenitor cells which express all three genes after transduction. The nucleic acid construct may include one or more unique restriction sites to facilitate further manipulation. In some embodiments, the nucleic acid construct may be introduced directly into T cells or progenitor cells using gene editing techniques. In other embodiments, the nucleic acid construct may be incorporated into an expression vector. Suitable vectors are well-known in the art and are described in more detail herein. Suitable vectors can be chosen or constructed, containing appropriate regulatory sequences, including promoter sequences, terminator fragments, polyadenylation sequences, enhancer sequences, marker genes and other sequences as appropriate. Preferably, the vector contains appropriate regulatory sequences to drive the expression of the nucleic acid in mammalian cells. A vector may also comprise sequences, such as origins of replication, promoter regions and selectable markers, which allow for its selection, expression and replication in bacterial hosts such as E. coli. Preferably, the nucleic acid construct is contained in a viral vector, most preferably a gamma retroviral vector or a lentiviral vector, such as a VSVg-pseudotyped lentiviral vector. The T cells may be transduced by contact with a viral particle comprising the nucleic acid. Viral particles for transduction may be produced according to known methods. For example, HEK293T cells may be transfected with plasmids encoding viral packaging and envelope elements as well as a lentiviral vector comprising the coding nucleic acid. A VSVg- pseudotyped viral vector may be produced in combination with the viral envelope glycoprotein G of the Vesicular stomatitis virus (VSVg) to produce a pseudotyped virus particle. A viral vector, such as a lentivirus, may be contained in a viral particle comprising the nucleic acid vector encapsulated by one or more viral proteins. A viral particle may be produced by a method comprising transducing mammalian cells with a viral vector as described herein and one or more viral packaging and envelope vectors and culturing the transduced cells in a culture medium, such that the cells produce lentiviral particles that are released into the medium. Following release of viral particles, the culture medium comprising the viral particles may be collected and, optionally the viral particles may be concentrated. Following production and optional concentration, the viral particles may be stored, for example by freezing at -80°C ready for use in transducing T cells or progenitor cells. The nucleic acid construct or vector may be introduced into the T cells or progenitor cells by any convenient method. Suitable methods for introducing or incorporating a heterologous nucleic acid into a T cell, certain considerations are well-known to those skilled in the art. The nucleic acid to be inserted may be assembled within a construct or vector which contains effective regulatory elements which will drive transcription in the T cell. Suitable techniques for transporting the construct or vector into the T cell are well known in the art and include calcium phosphate transfection, DEAE-Dextran, electroporation, liposome- mediated transfection and transduction using retrovirus or other virus, e.g. vaccinia or lentivirus. For example, solid-phase transduction may be performed without selection by culture on retronectin-coated, retroviral vector-preloaded tissue culture plates. Many known techniques and protocols for manipulation and transformation of nucleic acid, for example in preparation of nucleic acid constructs, introduction of DNA into cells and gene expression are described in detail in Protocols in Molecular Biology, Second Edition, Ausubel et al. eds. John Wiley & Sons, 1992. In some embodiments, the heterologous nucleic acid sequences may be introduced into T cells, for example T cells obtained from a donor individual, in order to produce a population of modified T cells expressing the heterologous nucleic acid sequences. In other embodiments, the heterologous nucleic acid sequences may be introduced into progenitor cells, such as induced pluripotent stem cells (iPSCs), mesoderm cells (MCs), haemogenic endothelial cells (HECs), haematopoietic progenitor cells (HPCs) or progenitor T cells. The progenitor cells may then be differentiated into T cells, in order to produce a population of modified T cells expressing the heterologous nucleic acid sequences. For example, a method of producing a modified population of T cells may comprise (i) differentiating a population of induced pluripotent stem cells (iPSCs) into mesoderm cells (MCs), (ii) differentiating the MCs to produce a population of haemogenic endothelial cells (HECs), (iii) differentiating the HECs into a population of haematopoietic progenitor cells (HPCs), (iv) differentiating the population of HPCs into progenitor T cells; and (v) maturing the progenitor T cells to produce a population of double positive CD4+ CD8+ T cells, wherein the method comprises (i) introducing a first heterologous nucleotide sequence encoding a T cell receptor (TCR) that binds to cancer cells expressing MAGE-A4 into any one of the iPSCs, MCs, HECs, HPCs or progenitor T cells; (ii) introducing a second heterologous nucleotide sequence encoding C-C motif chemokine ligand 19 (CCL19) into any one of the iPSCs, MCs, HECs, HPCs or progenitor T cells; and (iii) introducing a third heterologous nucleotide sequence encoding interleukin 7 (IL-7) into any one of the iPSCs, MCs, HECs, HPCs or progenitor T cells. In some embodiments, a method may comprise introducing the first, second and third nucleotide sequences into any one of the iPSCs, MCs, HECs, HPCs or progenitor T cells. The method may further comprise; (vi) activating and expanding the double positive CD4+ CD8+ T cells to produce a population of CD8+ T cells or a population of CD4+ T cells. Induced pluripotent stem cells (iPSCs) are pluripotent cells which are derived from non- pluripotent, fully differentiated donor or antecedent cells. iPSCs are capable of self-renewal in vitro and exhibit an undifferentiated phenotype and are potentially capable of differentiating into any foetal or adult cell type of any of the three germ layers (endoderm, mesoderm and ectoderm). The population of iPSCs may be clonal i.e. genetically identical cells descended from a single common ancestor cell. iPSCs may express one or more of the following pluripotency associated markers: POU5f1 (Oct4), Sox2, Alkaline Phosphatase, SSEA-3, Nanog, SSEA-4, Tra-1-60, KLF4 and c-myc, preferably one or more of POU5f1, NANOG and SOX2. An iPSC may lack markers associated with specific differentiative fates, such as Bra, Sox17, FoxA2, αFP, Sox1, NCAM, GATA6, GATA4, Hand1 and CDX2. In particular, an iPSC may lack markers associated with endodermal fates. Preferably, the iPSCs are human iPSCs (hiPSCs). IPSCs may be derived or reprogramed from donor cells, which may be somatic cells or other antecedent cells obtained from a source, such as a donor individual. The donor cells may be mammalian, preferably human cells. Suitable donor cells include adult fibroblasts and blood cells, for example peripheral blood cells, such as HPCs or mononuclear cells. Suitable donor cells for reprogramming into iPSCs as described herein may be obtained from a donor individual. In some embodiments, the donor individual may be the same person as the recipient individual to whom the T cells will be administered following production as described herein (autologous treatment). In other embodiments, the donor individual may be a different person to the recipient individual to whom the T cells will be administered following production as described herein (allogeneic treatment). For example, the donor individual may be a healthy individual who is human leukocyte antigen (HLA) matched (either before or after donation) with a recipient individual suffering from cancer. In other embodiments, the donor individual may not be HLA matched with the recipient individual. Preferably, the donor individual may be a neonate (new-born), for example the donor cells may be obtained from a sample of umbilical cord blood. In a first stage, iPSCs may be differentiated into mesoderm cells by culturing the population of iPSCs under suitable conditions to promote mesodermal differentiation. For example, the iPSCs cells may be cultured sequentially in first, second and third mesoderm induction media to induce differentiation into mesoderm cells. A suitable first mesoderm induction medium may stimulate SMAD2 and SMAD3 mediated signalling pathways. For example, the first mesoderm induction medium may comprise activin. A suitable second mesoderm induction medium may (i) stimulate SMAD1, SMAD2, SMAD3, SMAD5 and SMAD9 and/or SMAD1, SMAD2, SMAD3, SMAD5 and SMAD9 mediated signalling pathways and (ii) have fibroblast growth factor (FGF) activity. For example, the second mesoderm induction medium may comprise activin, preferably activin A, BMP, preferably BMP4 and FGF, preferably bFGF. A suitable third mesoderm induction medium may (i) stimulate SMAD1, SMAD2, SMAD3, SMAD5 and SMAD9 and/or SMAD1, SMAD2, SMAD3, SMAD5 and SMAD9 mediated signalling pathways (ii) have fibroblast growth factor (FGF) activity and (iii) inhibit glycogen synthase kinase 3β. For example, the third mesoderm induction medium may comprise activin, preferably activin A, BMP, preferably BMP4, FGF, preferably bFGF, and a GSK3 inhibitor, preferably CHIR99021. The first, second and third mesoderm induction media may be devoid of differentiation factors other than the differentiation factors set out above. In preferred embodiments, the first, second and third mesoderm induction media are chemically defined media. For example, the first mesoderm induction medium may consist of a chemically defined nutrient medium supplemented with an effective amount of activin, preferably activin A, for example 50ng/ml activin A; the second mesoderm induction medium may consist of a chemically defined nutrient medium supplemented with an effective amount of activin preferably activin A, for example 5ng/ml activin A, BMP, preferably BMP4, for example 10ng/ml BMP4; and FGF, preferably bFGF (FGF2), for example 5ng/ml bFGF; and the third mesoderm induction medium may consist of a chemically defined nutrient medium supplemented with an effective amount of activin preferably activin A, for example 5ng/ml activin A, BMP, preferably BMP4, for example 10ng/ml BMP4; FGF, preferably bFGF (FGF2), for example 5ng/ml bFGF; and GSK3 inhibitor, preferably CHIR-99021 , for example 10µM CHIR-99021. A chemically defined medium (CDM) is a nutritive solution for culturing cells which contains only specified components, preferably components of known chemical structure. A CDM is devoid of undefined components or constituents which include undefined components, such as feeder cells, stromal cells, serum, and complex extracellular matrices, such as matrigel ^TM For example, a CDM does not contain stromal cells, such as OP9 cells, expressing Notch ligands, such as DLL1 or DLL4. The 21hemicallly defined nutrient medium may comprise a chemically defined basal medium. Suitable chemically defined basal media include Iscove’s Modified Dulbecco’s Medium (IMDM), Ham’s F12, Advanced Dulbecco’s modified eagle medium (DMEM) (Price et al Focus (2003), 253-6), Williams E (Williams, G.M. et al Exp. Cell Research, 89, 139- 142 (1974)), RPMI-1640 (Moore, G.E. and Woods L.K., (1976) Tissue Culture Association Manual.3, 503-508) and StemPro ^TM -34 PLUS (ThermoFisher Scientific). The basal medium may be supplemented by serum-free culture medium supplements and/or additional components in the medium. Suitable supplements and additional components are described above and may include L-glutamine or substitutes, such as GlutaMAX-1 ^TM , ascorbic acid, monothiolglycerol (MTG), antibiotics such as penicillin and streptomycin, human serum albumin, for example recombinant human serum albumin, such as Cellastim ^TM (Merck/Sigma) and Recombumin ^TM (albumedix.com), insulin, transferrin and 2- mercaptoethanol. A basal medium may be supplemented with a serum substitute, such as Knockout Serum Replacement (KOSR; Invitrogen). The iPSCs may be cultured in the first mesoderm induction medium for 1 to 12 hours, for example any of 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11 or 12 hours, preferably about 4 hours; then cultured in the second mesoderm induction medium for 30 to 54 hours, for example any of 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49 or 50 hours, preferably about 44 hours; and then cultured in the third mesoderm induction medium for 36 to 60 hours, , for example any of 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52 or 53 hours, preferably about 48 hours to produce a population of mesodermal cells. Mesoderm cells are partially differentiated progenitor cells that are committed to mesodermal lineages and are capable of differentiation under appropriate conditions into all cell types in the mesenchyme (fibroblast), muscle, bone, adipose, vascular and haematopoietic systems. Mesoderm cells may express one or more mesodermal markers. For example, the mesoderm cells may express any one, two, three, four, five, six or all seven of Brachyury, Goosecoid, Mixl1, KDR, FoxA2, GATA6 and PDGFαR. In a second stage, mesoderm cells may be differentiated into haemogenic endothelial cells (HECs) by culturing the population of mesoderm cells under suitable conditions to promote haemogenic endothelial (HE) differentiation. For example, the iPSCs cells may be cultured in an HE induction medium. A suitable HE induction medium may (i) stimulate cKIT receptor (CD117) and/or cKIT receptor (CD117) mediated signalling pathways and (ii) stimulate VEGFR and/or VEGFR mediated signalling pathways. For example, the HE induction medium may comprise SCF and VEGF. In preferred embodiments, the HE induction medium is a chemically defined medium. For example, the HE induction medium may consist of a chemically defined nutrient medium supplemented with effective amounts of VEGF, for example 15ng/ml VEGF; and SCF, for example 100ng/ml SCF. Suitable chemically defined nutrient media are described above and include StemPro ^TM -34 (ThermoFisher Scientific). The mesoderm cells may be cultured in the HE induction medium for 2 to 6 days or 3 to 5 days, preferably about 4 days, to produce a population of HE cells. Haemogenic endothelial cells (HECs) are partially differentiated endothelial progenitor cells that have hematopoietic potential and are capable of differentiation under appropriate conditions into haematopoietic lineages. HE cells may express CD34. In some embodiments, HECs may not express CD73 or CXCR4 (CD184). For example, the HE cells may have the phenotype CD34+ CD73- or CD34+ CD73- CXCR4-. In a third stage, haemogenic endothelial (HE) cells may be differentiated into haematopoietic progenitor cells (HPCs) by culturing the population of HE cells under suitable conditions to promote haematopoietic differentiation. For example, the HE cells may be cultured in a haematopoietic induction medium. A suitable haematopoietic induction medium may stimulate the following (i) cKIT receptor (CD117) and/or cKIT receptor (CD117) mediated signalling pathways, (ii) VEGFR and/or VEGFR mediated signalling pathways, (iii) MPL (CD110) and/or MPL (CD110) mediated signalling pathways (iv) FLT3 and/or FLT3 mediated signalling pathways (v) IGF1R and/or IGF1R mediated signalling pathways (vi) SMAD1, 5 and 9 and/or SMAD1, 5 and 9 mediated signalling pathways (vii) Hedgehog and/or Hedgehog signalling pathways (viii) EpoR and/or EpoR mediated signalling pathway and (ix) AGTR2 and/or AGTR2 mediated signalling pathways. A suitable haematopoietic induction medium may also inhibit the AGTR1 (angiotensin II type 1 receptor (AT1)) and/or AGTR1 (angiotensin II type 1 receptor (AT1)) mediated signaling pathway. A suitable haematopoietic induction medium may also have interleukin (IL) activity and FGF activity. For example, a haematopoietic induction medium may comprise the differentiation factors: VEGF, SCF, Thrombopoietin (TPO), Flt3 ligand (Flt3L), IL-3, IL-6, IL-7, IL-11, IGF-1, BMP, FGF, Sonic hedgehog (SHH), erythropoietin (EPO), angiotensin II, and an angiotensin II type 1 receptor (AT1) antagonist. In preferred embodiments, the haematopoietic induction medium is a chemically defined medium. For example, the haematopoietic induction medium may consist of a chemically defined nutrient medium supplemented with effective amounts of VEGF, for example 15ng/ml; SCF, for example 100ng/ml; thrombopoietin (TPO), for example 30ng/ml; Flt3 ligand (FLT3L), for example 25ng./ml; IL-3, for example 25ng/ml; IL-6, for example 10ng/ml; IL-7, for example 10 ng/ml; IL-11, for example 5 ng/ml; IGF-1, for example 25 ng/ml; BMP, for example BMP4 at 10ng/ml; FGF, for example bFGF at 5ng/ml; Sonic hedgehog (SHH), for example 25ng/ml; erythropoietin (EPO), for example 2 u/ml; angiotensin II, for example 10µg/ml, and an angiotensin II type 1 receptor (AT1) antagonist, for example losartan, at 100µM. A suitable haematopoietic induction medium be devoid of other differentiation factors. For example, a haematopoietic induction medium may consist of a chemically defined nutrient medium supplemented with one or more differentiation factors, wherein the one or more differentiation factors consist of VEGF, SCF, Thrombopoietin (TPO), Flt3 ligand (Flt3L), IL-3, IL-6, IL-7, IL-11, IGF-1, BMP, FGF, Sonic hedgehog (SHH), erythropoietin (EPO), angiotensin II, and an angiotensin II type 1 receptor (AT ₁ ) antagonist (i.e. the medium does not contain any differentiation factors other than VEGF, SCF, Thrombopoietin (TPO), Flt3 ligand (Flt3L), IL-3, IL-6, IL-7, IL-11, IGF-1, BMP, FGF, Sonic hedgehog (SHH), erythropoietin (EPO), angiotensin II, and an angiotensin II type 1 receptor (AT ₁ ) antagonist). Suitable chemically defined nutrient media are described above and include StemPro ^TM -34 PLUS (ThermoFisher Scientific) or a basal medium such as IMDM supplemented with albumin, insulin, selenium transferrin, and lipids as described below. The HE cells may be cultured in the haematopoietic induction medium for 8-21 days, for example any of about 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 or 20 days, preferably about 16 days, to produce the population of HPCs. HPCs (also called hematopoietic stem cells) are multipotent stem cells that are committed to a hematopoietic lineage and are capable of further hematopoietic differentiation into all blood cell types including myeloid and lymphoid lineages, including monocytes, B cells and T cells. HPCs may express CD34. HPCs may co-express CD133, CD45 and FLK1 (also known as KDR or VEGFR2) and may be negative for expression of CD38 and other lineage specific markers. For example, HPCs may display the phenotype CD34+ CD133+ CD45+ FLK1+ CD38-. In a fourth stage, haematopoietic progenitor cells (HPCs) may be differentiated into progenitor T cells by culturing the population of HPCs under suitable conditions to promote lymphoid differentiation. For example, the haematopoietic progenitor cells may be cultured in a lymphoid expansion medium. A lymphoid expansion medium is a cell culture medium that promotes the lymphoid differentiation of HPCs into progenitor T cells. A suitable lymphoid expansion medium may (i) stimulate cKIT receptor (CD117; KIT receptor tyrosine kinase) and/or cKIT receptor (CD117; KIT receptor tyrosine kinase) mediated signalling pathways, (ii) stimulate MPL (CD110) and/or MPL (CD110) mediated signalling pathways (iii) FLT3 and/or FLT3 mediated signalling pathways and (iv) have interleukin (IL) activity. For example, a lymphoid expansion medium may comprise the differentiation factors SCF, FLT3L, TPO and IL7. In preferred embodiments, the lymphoid expansion medium is a chemically defined medium. For example, the lymphoid expansion medium may consist of a chemically defined nutrient medium supplemented with effective amounts of the above differentiation factors. Suitable lymphoid expansion media are well-known in the art and include Stemspan ^TM SFEM II (Cat # 9605; StemCell Technologies Inc, CA).with Stemspan ^TM lymphoid expansion supplement (Cat # 9915; StemCell Technologies Inc, CA). The HPCs may be cultured on a surface During differentiation into progenitor T cells. For example, the HPCs may be cultured on a surface of a culture vessel, bead or other biomaterial or polymer. Preferably, the surface may be coated with a factor that stimulates Notch signalling, for example a Notch ligand, such as Delta-like 1 (DLL1) or Delta-like 4 (DLL4). Suitable Notch ligands are well-known in the art and available from commercial suppliers. The surface may also be coated with an extracellular matrix protein, such as fibronectin, vitronectin, laminin or collagen and/or one or more cell surface adhesion proteins, such as VCAM1. In some embodiments, the surface for HPC culture may have a coating that comprises a factor that stimulates Notch signalling, for example a Notch ligand, such as DLL4, without the extracellular matrix protein or cell surface adhesion protein. In some embodiments, the surface for HPC culture may have a coating that comprises a factor that stimulates Notch signalling, for example a Notch ligand, such as DLL4, an extracellular matrix protein, such as vitronectin, and a cell surface adhesion protein, such as VCAM1. The surface may be coated with an extracellular matrix protein, factor that stimulates Notch signalling and cell surface adhesion protein by contacting the surface with a coating solution. For example, the coating solution may be incubated on the surface under suitable conditions to coat the surface. Conditions may, for example, include about 2 hours at room temperature. Coating solutions comprising an extracellular matrix protein and a factor that stimulates Notch signalling are available from commercial suppliers (StemSpan™ Lymphoid Differentiation Coating Material; Cat # 9925; Stem Cell Technologies Inc, CA). The HPCs may be cultured in the lymphoid expansion medium on the substrate or surface for a time sufficient for the HPCs to differentiate into progenitor T cells. For example, the HPCs may be cultured for 2-6 weeks, 2 to 5 weeks or 2-4 weeks, preferably 3 weeks. Progenitor T cells are multi-potent lymphopoietic progenitor cells that are capable of giving rise to αβ T cells, γδ T cells, tissue resident T cells and NK T cells. Progenitor T cells may commit to the αβ T cell lineage after pre-TCR selection in the thymus. Progenitor T cells may be capable of in vivo thymus colonization and may be capable of committing to the T cell lineage after pre-TCR selection in the thymus. Progenitor T cells may also be capable of maturation into cytokine-producing CD3 ⁺ T-cells. Progenitor T cells may express CD5 and CD7 i.e. the progenitor T cells may have a CD5+CD7+ phenotype. Progenitor T cells may also co-express CD44, CD25 and CD2. For example, progenitor T cells may have a CD5+, CD7+ CD44+, CD25+ CD2+ phenotype. In some embodiments, progenitor T cells may also co-express CD45. Progenitor T cells may lack expression of CD3, CD4 and CD8, for example on the cell surface. In a fifth stage, progenitor T cells may be matured into T cells by culturing the population of progenitor T cells under suitable conditions to promote T cell maturation. For example, the progenitor T cells may be cultured in a T cell maturation medium. A T cell maturation medium is a cell culture medium that promotes the maturation of progenitor T cells into mature T cells. A suitable T cell maturation medium may (i) stimulate cKIT receptor (CD117; KIT receptor tyrosine kinase) and/or cKIT receptor (CD117; KIT receptor tyrosine kinase) mediated signalling pathways (ii) FLT3 and/or FLT3 mediated signalling pathways and (iii) have interleukin (IL) activity. For example, a T cell maturation medium may comprise the differentiation factors SCF, FLT3L, and IL7. In preferred embodiments, the T cell maturation medium is a chemically defined medium. For example, the T cell maturation medium may consist of a chemically defined nutrient medium supplemented with effective amounts of the above differentiation factors. Suitable T cell maturation media are well-known in the art and include Stemspan ^TM SFEM II (Cat # 9605; StemCell Technologies Inc, CA) with Stemspan ^TM T cell maturation supplement (Cat # 9930; StemCell Technologies Inc, CA) and other media suitable for expansion of PBMCs and CD3+ cells, such as ExCellerate Human T cell expansion medium (R& D Systems, USA). Other suitable T cell maturation media may include a basal medium such as IMDM, supplemented with ITS, albumin and lipids, as described elsewhere herein and further supplemented with effective amounts of the above differentiation factors. The progenitor T cells may be cultured on a surface. For example, the progenitor T cells may be cultured on a surface of a culture vessel, bead or other biomaterial or polymer. Preferably, the surface may be coated with a factor that stimulates Notch signalling, for example a Notch ligand, such as Delta-like 1 (DLL1) or Delta-like 4 (DLL4). Suitable Notch ligands are well-known in the art and available from commercial suppliers. The surface may also be coated with an extracellular matrix protein, such as fibronectin, vitronectin, laminin or collagen and/or one or more cell surface adhesion proteins, such as VCAM1. Suitable coatings are well-known in the art and described elsewhere herein. The progenitor T cells may be cultured in the T cell maturation medium on the substrate or surface for a time sufficient for the progenitor T cells to mature into T cells. For example, the progenitor T cells may be cultured for 1-4 weeks, preferably 2 or 3 weeks. Suitable methods for the production of T cells from progenitor cells, such as iPSCs, are described in WO2021/032852, WO2021/032855, WO2021/032851, WO2021/032836, WO2022/175401 and WO2021/229212. Following the introduction of nucleic acid into the T cells or T cell progenitors, the initial population of modified T cells may be cultured in vitro such that the modified T cells proliferate and expand the population. The modified T cell population may for example be expanded using magnetic beads coated with anti-CD3 and anti-CD28. The modified T cells may be cultured using any convenient technique to produce the expanded population. Suitable culture systems include stirred tank fermenters, airlift fermenters, roller bottles, culture bags or dishes, and other bioreactors, in particular hollow fibre bioreactors. The use of such systems is well-known in the art. Numerous culture media suitable for use in the proliferation of T cells ex vivo are available, in particular complete media, such as AIM-V, Iscoves medium and RPMI-1640 (Invitrogen- GIBCO). The medium may be supplemented with other factors such as serum, serum proteins and selective agents. For example, in some embodiments, RPMI-1640 medium containing 2 mM glutamine, 10% FBS, 25 mM HEPES, pH 7.2, 1% penicillin-streptomycin, and 55 μM β-mercaptoethanol and optionally supplemented with 20 ng/ml recombinant IL-2 may be employed. The culture medium may be supplemented with the agonistic or antagonist factors described above at standard concentrations which may readily be determined by the skilled person by routine experimentation. Conveniently, cells are cultured at 37°C in a humidified atmosphere containing 5% CO2 in a suitable culture medium. Methods and techniques for the culture of T cells and other mammalian cells are well-known in the art (see, for example, Basic Cell Culture Protocols, C. Helgason, Humana Press Inc. U.S. (15 Oct 2004) ISBN: 1588295451; Human Cell Culture Protocols (Methods in Molecular Medicine S.) Humana Press Inc., U.S. (9 Dec 2004) ISBN: 1588292223; Culture of Animal Cells: A Manual of Basic Technique, R. Freshney, John Wiley & Sons Inc (2 Aug 2005) ISBN: 0471453293, Ho WY et al J Immunol Methods. (2006) 310:40-52). In some embodiments, it may be convenient to isolate and/or purify the modified T cells from the population. Any convenient technique may be used, including FACS and antibody coated magnetic particles. Optionally, the population of modified T cells produced as described herein may be stored, for example by lyophilisation and/or cryopreservation, before use. A population of modified T cells may be admixed with other reagents, such as buffers, carriers, diluents, preservatives and/or pharmaceutically acceptable excipients. Suitable reagents are described in more detail below. A method described herein may comprise admixing the population of modified T cells with a pharmaceutically acceptable excipient. Pharmaceutical compositions suitable for administration (e.g. by infusion), include aqueous and non-aqueous isotonic, pyrogen-free, sterile injection solutions which may contain anti- oxidants, buffers, preservatives, stabilisers, bacteriostats, and solutes which render the formulation isotonic with the blood of the intended recipient; and aqueous and non-aqueous sterile suspensions which may include suspending agents and thickening agents. Examples of suitable isotonic vehicles for use in such formulations include Sodium Chloride Injection, Ringer’s Solution, or Lactated Ringer’s Injection. Suitable vehicles can be found in standard pharmaceutical texts, for example, Remington’s Pharmaceutical Sciences, 18 ^th edition, Mack Publishing Company, Easton, Pa., 1990. In some preferred embodiments, the modified T cells may be formulated into a pharmaceutical composition suitable for intravenous infusion into an individual. The term “pharmaceutically acceptable” as used herein pertains to compounds, materials, compositions, and/or dosage forms which are, within the scope of sound medical judgement, suitable for use in contact with the tissues of a subject (e.g., human) without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit/risk ratio. Each carrier, excipient, etc. must also be “acceptable” in the sense of being compatible with the other ingredients of the formulation. Other aspects of the invention provide a population of modified T cells expressing a nucleic construct or a vector as described herein and a population of T cells that express a heterologous TCR that binds to MAGE A4 expressing cancer cells and further express heterologous IL-7 and CCL19. The T cells may bind specifically to cancer cells that express MAGE A4. A suitable population may be produced by a method described above. The population of modified T cells may be for use as a medicament. For example, a population of modified T cells as described herein may be used in cancer immunotherapy therapy, for example adoptive T cell therapy. Other aspects of the invention provide the use of a population of modified T cells as described herein for the manufacture of a medicament for the treatment of cancer, a population of modified T cells as described herein for use in the treatment of cancer, and a method of treatment of cancer may comprise administering a population of modified T cells as described herein to an individual in need thereof. Modified T cells that express IL-7 and CCL19 as described herein may display one or more of improved T-cell engraftment, functionality, and/or immune cell infiltration into a tumor relative to T cells that do not express IL-7 and CCL19. The heterologous TCR expressed by the T cells may specifically bind to the cancer cells of a cancer patient. The cancer patient may be subsequently treated with the modified T cells. Suitable cancer patients for treatment with the modified T cells may be identified by a method comprising; obtaining sample of cancer cells from an individual with cancer and; identifying one or more of the cancer cells in the sample to be MAGE A4 expressing cancer cells. Cancer cells identified as expressing MAGE A4 may bind to the TCR expressed by the modified T cells. Cancer cells may be identified as binding to the TCR encoded by the third nucleotide sequence by identifying the expression of MAGE A4 by the cancer cells. Methods of identifying antigens on the surface of cancer cells obtained from an individual with cancer are well-known in the art. The cancer cells of an individual suitable for treatment as described herein may express MAGE A4 and may be of correct HLA type to bind the TCR expressed by the T cell (for example the cells may be HLA-A*-201). Cancer cells may be distinguished from normal somatic cells in an individual by the expression of MAGE A4 tumour antigen. Normal somatic cells in an individual may not express MAGE A4 or may express it in a different manner, for example at lower levels, in different tissue and/or at a different developmental stage. The population of modified T cells may be autologous i.e. the modified T cells were originally obtained from the same individual to whom they are subsequently administered (i.e. the donor and recipient individual are the same). A suitable population of modified T cells for administration to the individual may be produced by a method comprising providing an initial population of T cells obtained from the individual, modifying the T cells to inducibly express IL-7 and constitutively express an antigen receptor which binds specifically to cancer cells in the individual as described herein, and culturing the modified T cells. The population of modified T cells may be allogeneic i.e. the modified T cells were originally obtained from a different individual to the individual to whom they are subsequently administered (i.e. the donor and recipient individual are different). The donor and recipient individuals may be HLA matched to avoid GVHD and other undesirable immune effects. A suitable population of modified T cells for administration to a recipient individual may be produced by a method comprising providing an initial population of T cells obtained from a donor individual, modifying the T cells to inducibly express IL-7 and constitutively express an antigen receptor which binds specifically to cancer cells in the recipient individual, as described herein, and culturing the modified T cells. Following administration of the modified T cells, the recipient individual may exhibit a T cell mediated immune response against cancer cells in the recipient individual. This may have a beneficial effect on the cancer condition in the individual. Cancer conditions may be characterised by the abnormal proliferation of malignant cancer cells. Preferred cancer conditions for treatment as described herein may include solid cancers or solid tumours, such as sarcomas, including synovial sarcomas and myxoid/round cell liposarcoma (MRCLS), skin cancer, melanoma, bladder cancer, brain cancer, breast cancer, uterus cancer, urothelial cancer, ovarian cancer, including metastatic ovarian cancer, prostate cancer, lung cancer, including metastatic lung cancer, lung carcinoid cancer, small cell lung cancer, and non- small cell lung cancer (NSCLC), such as adenocarcinoma, squamous cell carcinoma, adenosquamous carcinoma and large cell carcinoma, and metastatic or advanced NSCLC, colorectal cancer, including colorectal carcinoma, colorectal adenocarcinoma and metastatic colorectal cancer, cervical cancer, liver cancer, including metastatic liver cancer, head and neck cancer, including head and neck SCC (squamous cell carcinoma), oesophageal cancer, esophagogastric junction cancer (EGJ), pancreatic cancer, including metastatic pancreatic cancer, pancreatic carcinoma, pancreatic adenocarcinoma, mucinous adenoma, and ductal carcinoma of the pancreas, renal cancer, adrenal cancer, stomach cancer, including metastatic stomach cancer, gastric cancer, including metastatic gastric cancer, testicular cancer, cancer of the gall bladder and biliary tracts, thyroid cancer, endometrial cancer, thymus cancer, cancer of bone, and cerebral cancer, as well as cancer of unknown primary (CUP). The cancer may also include haematologic malignancies such as acute myeloid leukaemia (AML), chronic myeloid leukaemia (CML), myelodysplastic syndrome (MDS), acute lymphocytic leukaemia (ALL), chronic lymphocytic leukaemia (CLL), adult T-cell leukaemia (ATL), and lymphoma (including Hodgkin lymphoma and non-Hodgkin lymphoma). In some embodiments, suitable cancers may express a tumour antigen, such as MAGE A4. In some embodiments, suitable cancers may also express a PD-1 ligand, such as PD-L1. Cancer cells within an individual may be immunologically distinct from normal somatic cells in the individual (i.e. the cancerous tumour may be immunogenic). For example, the cancer cells may be capable of eliciting a systemic immune response in the individual against one or more antigens expressed by the cancer cells, such as MAGE A4. The tumour antigens that elicit the immune response may be specific to cancer cells or may be shared by one or more normal cells in the individual. An individual suitable for treatment as described above may be a mammal, such as a rodent (e.g. a guinea pig, a hamster, a rat, a mouse), murine (e.g. a mouse), canine (e.g. a dog), feline (e.g. a cat), equine (e.g. a horse), a primate, simian (e.g. a monkey or ape), a monkey (e.g. marmoset, baboon), an ape (e.g. gorilla, chimpanzee, orang-utan, gibbon), or a human. In preferred embodiments, the individual is a human. In other preferred embodiments, non- human mammals, especially mammals that are conventionally used as models for demonstrating therapeutic efficacy in humans (e.g. murine, primate, porcine, canine, or rabbit animals) may be employed. In some embodiments, the individual may have minimal residual disease (MRD) after an initial cancer treatment. An individual with cancer may display at least one identifiable sign, symptom, or laboratory finding that is sufficient to make a diagnosis of cancer in accordance with clinical standards known in the art. Examples of such clinical standards can be found in textbooks of medicine such as Harrison’s Principles of Internal Medicine, 15 ^th Ed., Fauci AS et al., eds., McGraw- Hill, New York, 2001. In some instances, a diagnosis of a cancer in an individual may include identification of a particular cell type (e.g. a cancer cell) in a sample of a body fluid or tissue obtained from the individual. Treatment may be any treatment and therapy, whether of a human or an animal (e.g. in veterinary applications), in which some desired therapeutic effect is achieved, for example, the inhibition or delay of the progress of the condition, and includes a reduction in the rate of progress, a halt in the rate of progress, amelioration of the condition, cure or remission (whether partial or total) of the condition, preventing, delaying, abating or arresting one or more symptoms and/or signs of the condition or prolonging survival of a subject or patient beyond that expected in the absence of treatment. Treatment may also be prophylactic (i.e. prophylaxis). For example, an individual susceptible to or at risk of the occurrence or re-occurrence of cancer may be treated as described herein. Such treatment may prevent or delay the occurrence or re-occurrence of cancer in the individual. Treatment may include inhibiting cancer growth, including complete cancer remission, and/or inhibiting cancer metastasis. Cancer growth generally refers to any one of a number of indices that indicate change within the cancer to a more developed form. Thus, indices for measuring an inhibition of cancer growth include a decrease in cancer cell survival, a decrease in tumour volume or morphology (for example, as determined using computed tomographic (CT), sonography, or other imaging method), a delayed tumour growth, a destruction of tumour vasculature, improved performance in delayed hypersensitivity skin test, an increase in the activity of T cells, and a decrease in levels of tumour-specific antigens. Administration of T cells modified as described herein may improve the capacity of the individual to resist cancer growth, in particular growth of a cancer already present the subject and/or decrease the propensity for cancer growth in the individual. The modified T cells or the pharmaceutical composition comprising the modified T cells may be administered to a subject by any convenient route of administration, whether systemically/ peripherally or at the site of desired action, including but not limited to; parenteral, for example, by infusion. Infusion involves the administration of the T cells in a suitable composition through a needle or catheter. Typically, T cells are infused intravenously or subcutaneously, although the T cells may be infused via other non-oral routes, such as intramuscular injections and epidural routes. Suitable infusion techniques are known in the art and commonly used in therapy (see, e.g., Rosenberg et al., New Eng. J. of Med., 319:1676, 1988). Typically, the number of cells administered is from about 10 ⁵ to about 10 ¹⁰ per Kg body weight, typically 2x10 ⁸ to 2x10 ¹⁰ cells per individual, typically over the course of 30 minutes, with treatment repeated as necessary, for example at intervals of days to weeks. It will be appreciated that appropriate dosages of the modified T cells, and compositions comprising the modified T cells, can vary from patient to patient. Determining the optimal dosage will generally involve the balancing of the level of therapeutic benefit against any risk or deleterious side effects of the treatments of the present invention. The selected dosage level will depend on a variety of factors including, but not limited to, the activity of the particular cells, the route of administration, the time of administration, the rate of loss or inactivation of the cells, the duration of the treatment, other drugs, compounds, and/or materials used in combination, and the age, sex, weight, condition, general health, and prior medical history of the patient. The amount of cells and the route of administration will ultimately be at the discretion of the physician, although generally the dosage will be to achieve local concentrations at the site of action which achieve the desired effect without causing substantial harmful or deleterious side-effects. While the modified T cells may be administered alone, in some circumstances the modified T cells may be administered in combination with the target antigen, APCs displaying the target antigen, and/or IL-2 to promote expansion in vivo of the population of modified T cells. The population of modified T cells may be administered in combination with one or more other therapies, such as cytokines e.g. IL-2, cytotoxic chemotherapy, radiation and immuno- oncology agents, including checkpoint inhibitors, such as anti-B7-H3; anti-B7-H4; anti-TIM3; anti-KIR; anti-LAG3; PD-1 axis inhibitors, such as anti-PD-1, and anti-PD-L1; and anti- CTLA4 antibodies. In some preferred embodiments, the population of modified T cells may be administered in combination with a PD-1 axis inhibitor. Suitable PD-1 axis inhibitors may include anti-PD-1 and anti-PD-L1 antibodies, such as nivolumab and pembrolizumab. The one or more other therapies may be administered by any convenient means, preferably at a site which is separate from the site of administration of the modified T cells. Administration of modified T cells can be effected in one dose, continuously or intermittently (e.g., in divided doses at appropriate intervals) throughout the course of treatment. Methods of determining the most effective means and dosage of administration are well known to those of skill in the art and will vary with the formulation used for therapy, the purpose of the therapy, the target cell being treated, and the subject being treated. Single or multiple administrations can be carried out with the dose level and pattern being selected by the treating physician. Preferably, the modified T cells are administered in a single transfusion of a least 1 x 10 ⁹ T-cells. The features disclosed in the foregoing description, or in the following claims, or in the accompanying drawings, expressed in their specific forms or in terms of a means for performing the disclosed function, or a method or process for obtaining the disclosed results, as appropriate, may, separately, or in any combination of such features, be utilised for realising the invention in diverse forms thereof. It is to be understood that the application discloses all combinations of any of the above aspects and embodiments described above with each other unless the context demands otherwise. Similarly, the application discloses all combinations of the preferred and/or optional features either singly or together with any of the other aspects, unless the context demands otherwise. It must be noted that, 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. Ranges may 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 the use of the antecedent “about,” it will be understood that the particular value forms another embodiment. Modifications of the above embodiments, further embodiments and modifications thereof will be apparent to the skilled person on reading this disclosure, and as such, these are within the scope of the present invention. All documents and sequence database entries mentioned in this specification are incorporated herein by reference in their entirety for all purposes. “and/or” where used herein is to be taken as specific disclosure of each of the two specified features or components with or without the other. For example, “A and/or B” is to be taken as specific disclosure of each of (i) A, (ii) B and (iii) A and B, just as if each is set out individually herein. Other aspects and embodiments of the invention provide the aspects and embodiments described above with the term “comprising” replaced by the term “consisting of” and the aspects and embodiments described above with the term “comprising” replaced by the term ”consisting essentially of”. Certain aspects and embodiments of the invention will now be illustrated by way of example and with reference to the figures described above. Experiments Methods Effector Cells G-Rex ‘Wave’ T-cell products from three donors will be used for these experiments, namely: Wave266, Wave267 and Wave268. For each donor, non-transduced (ntd) T cells, ADP- A2M4 TCR alone and ADP-A2M4N7X19 transduced T-cells were tested. T-cells were thawed on the day of the assay and rested for at least 1 hour in R10 media at 37 ⁰C/5 % CO2 prior inclusion in the assay. The TCR constructs under investigation, along with the donor codes are listed in Table 1. The HLA-A2 status of the donors is shown in Table 2. Table 1 Plasmid/ADB code TCR/Construct Name Table 2 Target Cells The HLA-A*02:01 and MAGEA4 antigen positive cell line NCI-H1755 was used to present antigen to T-cells. Endothelial cells Primary human dermal microvascular endothelial cells (HDMEC7) were included in the Transwell assays to aid the migration of DCs from the upper to lower chamber. They were plated 72 hours prior to assay set up in the upper chambers of the Transwell plates onto a gelatin matrix. Migratory Cells DCs were isolated from the whole blood of two donors. The CD14+ fraction of PBMCs were isolated by magnetic bead separation and cultured in phenol red-free R10 for 6 days in the presence of IL-4 & GM-CSF, to generate immature DCs (iDCs) according to CBP 054v03. 48 hours before assay set-up, immature DCs were treated with a cytokine cocktail to induce maturation. Restimulation Assay Target cells were cultured according to CBP 002v03 and thawed from assay ready vials on the day prior to co-culture set-up. Target cells were washed and resuspended in 5 mL R10 prior to irradiation at 48 Gy. Target cells were resuspended at 1x10 ⁶ cells/mL prior to plating for the assay. For the conditions with exogenous rhIL-7, 20 ng/mL of rhIL-7 was added at twice the concentration to the appropriate number of A375 cells, prior to plating. ADP-A2M4, ADP-A2M4N7X19 and ntd T-cells from three different donors (Wave266, Wave267 and Wave 268; one per assay) were thawed and rested in 30 mL of pre-warmed R10 and rested for at least 2 hours. Cells were pelleted by centrifugation at 1000 rpm for 5 minutes and resuspended in 10 mL of R10 for cell counting. T-cell counting was performed using flow cytometry. T-cells were resuspended to 1x10 ⁶ cells/mL and plated out in an appropriate cell culture vessel with the irradiated targets at a ratio of 1:1. Co-cultures were incubated for 7 days. On the 7 ^th day, all conditions were harvested and counted by flow cytometry in the same way as before. After an accurate T-cell count was determined, they were then resuspended back to 1x10 ⁶ cells/mL plated out in an appropriate cell culture vessel with a fresh batch of irradiated A375s (prepared as above). On day 7 an antigen removal condition was setup in which T-cells were plated out as before but with an equivalent volume of R10 alone added. Stimulations in this manner were repeated until day 28. Flow Cytometry and Cell Counting The Attune NxT Flow Cytometer was used to count and phenotype the T-cells over the course of the assay. Briefly, 60 µL of T-cells (PSPdev015) were transferred into a 96-well u- bottom plate and incubated with a cocktail of antibodies, as listed in Table 3. Cells were then incubated at 4°C for 15 minutes prior to the addition of the CountBright™ counting beads. CountBright™ counting beads were warmed to room temperature and vortexed for 30 seconds to evenly resuspend them. Immediately after vortexing, 60 µL (PSPdev015) of the bead suspension was added to each sample to be counted. Tube volume was then topped up to 300 µL with FACS buffer and the samples analysed. A fluorescent minus one (FMO) panel was used to inform the gate voltages and gating was performed according to the strategies detailed in the appendix (section 7.3.1). Absolute T- cell counts were determined using lymphocyte common antigen (CD45) marker and counting beads. Absolute T-cell counts per μL were then calculated using the following formula: Immunophenotyping analysis assessing the frequency of expression of CD8, CCR7, CD45 RA and CD45 RO was performed using the same samples. Fold change calculations Fold change in T-cell number was calculated by dividing the concentration of cells after restimulation by the concentration before restimulation. Briefly, absolute cell counts were determined (CD45+ T cells/mL) by flow cytometry and used to seed T-cells at a final density of 0.5 x 10 ⁶ CD45+ T cells/mL. After 7 days the samples were harvested, and an absolute count determined (CD45+ T cells/mL) in the same way. Fold change from day 0 was then inferred over the course of the assay by multiplying subsequent weeks together. The fold change in T-cell subsets was determined by applying the phenotyping frequency data to the absolute counts of CD45+ T-cells as appropriate. Supernatant Collection Supernatants were collected over the course of the assay, before restimulation and 24 hours afterwards (days: 1, 7, 814, 15, 21, 22 and 28). Where multiple wells for a single condition existed, supernatants were pooled prior to storage. Supernatants were stored at -80 °C prior to thawing for cytokine analysis by supernatant ELISA or MSD™ Multi Spot Assay. Meso Scale Discovery™ Multi Spot Assay System Supernatants were analysed using the Meso Scale Discovery™ (MSD™) Multi Spot Assay System according to the manufacturer’s instructions. Two panels of analytes were used. The MSD™ Human Cytokine Panel 1 V-PLEX kit (10 analytes) and the Human Proinflammatory Panel 1 V-PLEX kit (10 analytes). Briefly, samples were thawed and diluted with MSD™ Diluent 100 prior to dilution with the appropriate Calibrator Diluent. Each sample was run in duplicate wells. Readings were acquired using a MESO QuickPlex SQ120 Electrochemiluminescence (ECL), using acquisition software Methodical Mind version 4.2. ECL data was exported and analysed within the Discovery Workbench software version 4.0. Readings falling below the respective lower standard curve limit were ascribed the minimal standard curve value for data plotting interpretation and analysis. While cytokine values that fell above the respective upper standard curve limit were ascribed the maximal standard curve value (multiplied by dilution factor) for data plotting interpretation and analysis. Where necessary replicate supernatants were run in further assays at different dilutions to bring the signals into range. Data was subsequently analysed and plotted using an R-script. CCL19 supernatant ELISA Supernatants were analysed using the R&D systems human CCL19/MIP-3 beta DuoSet ELISA kit (cat# DY461). Briefly, samples were thawed and diluted 1 in 10 or 1 in 20 with 1 % BSA reagent diluent. Each sample was run in at least duplicate wells and readings were acquired using the BMG OMEGA plate reader (serial number 415.2141). Readings falling below the respective lower standard curve limit were ascribed a value of 0 for data plotting interpretation and analysis. While cytokine values that fell above the respective upper standard curve limit were ascribed the maximal standard curve value (multiplied by dilution factor) for data plotting interpretation and analysis. Data was analysed in the first instance using the in house Adaptiplot Shiny App prior to plotting for the report using an R-script. Immunophenotyping Immunophenotyping was performed by flow cytometry on day 7 (24 hours after the addition of the maturation cytokine cocktail, 24 hours before use in the Transwell migration assay) to confirm a mature status of dendritic cells using a panel of antibodies. Transwell migration assay Transwell migration assays were performed to assess the chemotactic ability of ADP- A2M4N7X19 compared to ADP-A2M4 and ADP-A2M4IL7. Briefly, endothelial cells were grown on top of a light-impermeable 3 µM filter that separates two chambers. CMFDA (green fluorescent dye) labelled mature DCs (mDCs) were added to the upper chamber and either a chemoattractant (rhCCL19), or a target/effector co-culture was added to the lower chamber. The fluorescence of mDCs that had migrated across the endothelial cells and through the filter was measured by a Fluostar plate reader as a measure of the number of cells migrating across the membrane. Inserts were coated with human dermal microvascular endothelial cells (HDMEC) that were grown to confluence for 72 hrs. Co-cultures containing targets and effectors were plated into the lower chamber 48 hrs before the assay. Targets had been irradiated at 48 Gy and washed 1x in R10 prior to plating out. All three donors were tested, and each combination of effector/target was set up in triplicate. On assay day, mDCs were counted (as described in CBP 067v00) and resuspended in 2.5 µM CMFDA for 40 minutes at 37°C. They were then washed in PBS and resuspended to 10x106cells/mL in phenol red free R10 so that 5x105cells were dispensed in 50 µL.100 ng/mL rhCCL19 was included as a positive control. Plates were kept at 37°C / 5% CO2 for the duration of the assay and the fluorescence of CMFDA labelled DCs that had migrated to the lower chambers was measured every 30 minutes for 6 hours. Mean fluorescent units are the raw values captured by the plate reader, these were blank-corrected (values from blank wells subtracted from all other wells) (PSPdev022) and triplicate wells per condition were averaged and SEM calculated in Excel. Data was plotted in GraphPad Prism. CCL19 supernatant ELISA Supernatants from the co-cultures were collected, diluted 1/5 and the concentration of CCL19 produced was determined by ELISA. Data from CCL19/MIP-3β supernatant ELISA assays were acquired on a Fluostar plate reader (BMG), and raw values converted to CCL19 by comparison to internal standard curves using an Adaptiplot Data Analysis app. Results Constructs The secretion of IL-7 and CCL19 was tested in T cells transfected with different constructs. The highest levels of secretion were observed for the construct (ADB02651) in which the genes are in the order TCR_CCL19_IL-7 and driven by a constitutive promoter (Figure 10). The lowest levels of secretion were observed for the construct (ADB02655) in which the genes are in the order TCR_IL-7_CCL19 and driven by an inducible promoter. Cell Counting Afamitresgene autoleucel (previously known as ADP-A2M4) T cells express a MAGEA4 specific TCR without IL-7 and CCL19. ADP-A2M4N7X19 T cells were generated by additionally co-expressing recombinant IL-7 and CCL19 in the afamitresgene autoleucel T cells. To determine if the addition of IL-7 (and CCL19) to afamitresgene autoleucel (ADP-A2M4) improves the ability of ADP-A2M4N7X19 to survive or even proliferate in the presence of antigen, afamitresgene autoleucel, ADP-A2M4N7X19 and non-transduced T-cells were restimulated with irradiated A375 (MAGE-A4 antigen-positive) cells on a weekly basis for a total of 28 days. At each restimulation timepoint, cells were analysed by flow cytometry using a small panel of antibodies that included counting beads. Antigen restimulation occurred every 7 days (until day 28), counts were assessed by flow cytometry. For all three T-cell donors, ADP-A2M4N7X19 expanded over the course of the 28-day restimulation assay with some donor variation (Figure 1). In contrast, afamitresgene autoleucel expanded to a lesser extent and only until day 14 before declining, while non- transduced T-cell products declined in number over the entire course of the assay. The addition of exogenous rhIL-7 resulted in expansion of both afamitresgene autoleucel and ADP-A2M4N7X19 T-cells, with no expansion of the non-transduced T-cells (Figure 1). These data indicate that improved survival and proliferation of the ADP-A2M4N7X19 is IL-7 and antigen-dependent. Frequencies of CD8 and TCR-positive and -negative T-cell subsets at each time point were also captured by flow cytometry (Figure 2). The expansion of CD8 ⁺ T-cell subsets appear to be TCR-independent as cell counts of the TCR-negative fraction increased to a similar extent, or greater than CD8 ⁺ /TCR ⁺ over the 28-day period. This indicates that in vivo ADP- A2M4N7X19 supports the survival and proliferation of other tumor infiltrating lymphocytes in the tumor microenvironment and allow the possibility for epitope spreading. To determine whether the removal of target antigen prevents ADP-A2M4N7X19 transduced T-cell proliferation, parallel plates containing cells from 2 donors without A375 (MAGE-A4 antigen-positive) cells was prepared at day 7 (Figure 3, dotted line). As expected, the removal of antigen resulted in the decline of ADP-A2M4N7X19 T-cell populations in both donors. The addition of exogenous rhIL-7 had minimal effect on T-cell persistence after antigen removal (bottom panels), suggesting that T-cells need both antigen exposure and IL- 7 signalling for survival. This is an important observation to support the safety of ADP- A2M4N7X19. Cytokine Profiling At each time point for the assays detailed above, supernatants were taken both before and 24 hours after restimulation with antigen and stored for subsequent analysis for a range of cytokines (Table 6) by Meso Scale Discovery (MSD) multiplex assays. For each timepoint, the level of each cytokine detected in the presence of exogenous rhIL-7 was measured (data not shown). CCL19 secretion was measured by a separate ELISA. Comparable levels of IFNγ were detected in the supernatants of both afamitresgene autoleucel and ADP-A2M4N7X19 at Day 1 and Day 7, with Day 1 values elevated compared to Day 7 (Figure 4). For subsequent antigen stimulations, IFNγ levels were consistently higher for ADP-A2M4N7X19 T-cells. Sustained IFNγ production throughout the duration of the assay indicates that IL-7 reduces T-cell exhaustion from repeated stimulation. As expected, negligible IL-7 and CCL19 were detected with the non-transduced T-cells and afamitresgene autoleucel. In contrast, ADP-A2M4N7X19 had sustained IL-7 (Figure 5) and CCL19 (Figure 6) production throughout the duration of the restimulation assay, in line with IFNγ data. Further cytokines were also evaluated and no responses of concern were observed. In summary, the response of ADP-A2M4N7X19 to repeated antigen stimulation was assessed by measuring cell expansion and cytokine release. ADP-A2M4N7X19 demonstrated: ^ An enhanced ability to respond to repeated antigen stimulations up to at least 2 weeks longer than afamitresgene autoleucel. ^ Expansion of IL-7-induced CD8+ TCR- population allowing the possibility of epitope spreading. ^ Secretion of higher levels of proinflammatory cytokines such as IFNγ, than afamitresgene autoleucel. ^ Antigen-dependency of cytokine release and expansion. ^ No difference from afamitresgene autoleucel in the phenotype of memory T-cells, except between donor and assay conditions. ^ IL-7 production after clinical dosing was estimated to result in a steady-state concentration range between 436 – 981 pg/mL. The greater of these estimated values is 1.7-1.8-fold lower than Cmax values reported from systemic IL-7 therapy in clinical studies. Immune Cell Migration Towards ADP-A2M4N7X19 The CCL19 element of ADP-A2M4N7X19 is intended to improve local trafficking of T-cells and other immune cells into solid tumours. To confirm production of CCL19 by ADP- A2M4N7X19 has the intended effect, a transwell migration assay was developed. These assays were designed to mimic the gradient of CCL19 secretion that may be found in the tumor microenvironment. The transwell migration assay measures the chemotactic ability of cells toward a chemo- attractant. In this case, the ability of CCL19 released by ADP-A2M4N7X19 T-cells to act as a chemo-attractant. ADP-A2M4N7X19 were plated with NCI-H1755 (MAGE-A4 antigen- positive) cells in the bottom chamber of a transwell plate, with stimulation leading to the release of CCL19. Mature dendritic cells (mDCs) were used as migratory cells because they highly express CCR7 (the receptor for CCL19) and play a key role in antitumor immunity. Controls included recombinant human (rh)-CCL19 as chemo-attractant control and ADP- A2M4IL7 (T-cells that express IL-7 under an inducible, rather than a constitutive, promoter as in ADP-A2M4N7X19). Migration of fluorescently stained mDCs was quantified as mean fluorescent units measured in the lower chamber of the transwell. Only background migration was observed for non-transduced, afamitresgene autoleucel, and ADP-A2M4IL7 T-cells (Figure 7). The migration rate and peak migration of mDCs in the presence of ADP-A2M4N7X19 and rhCCL19 are very similar, even though the concentration of rhCCL19 used was ~10 fold greater than the CCL19 measured in the supernatants of ADP-A2M4N7X19 T-cells/targets The lack of mDC migration towards activated ADP- A2M4IL7 indicates that the migration observed for ADP-A2M4N7X19 is due to expression of CCL19. These experiments assessing the ability of ADP-A2M4N7X19 to induce mature DC migration in a transwell system displayed an increased ability of ADP-A2M4N7X19 to induce immune cell migration compared to afamitresgene autoleucel as a consequence of CCL19 production upon T-cell stimulation. Cytotoxic Potency IncuCyte killing assays were performed to analyze effector functions of nontransduced T- cells, afamitresgene autoleucel, and ADP-A2M4N7X19 in response to short-term antigen stimulation, to confirm that the addition of IL-7 and CCL19 functionality does not impair the short-term cytotoxic potency of the SPEAR T-cells. No difference in the rate of overall killing was seen between afamitresgene autoleucel and ADP-A2M4N7X19 T-cells (Figure 8). This demonstrates that the addition of IL-7 and CCL19 expression does not impact the short-term killing capability of afamitresgene autoleucel. In vivo Mouse Model An in vivo syngeneic mouse model was performed to determine the antitumor benefits of IL- 7 and CCL19 expression in conjunction with a TCR, and to assess the relative benefit of IL-7 and CCL19 expressed under a constitutive or inducible promoter. While it is possible to perform efficacy studies using the intended human clinical product in immune-deficient animal models, as were performed for ADP-A2M4, these would not provide additional information on ADP-A2M4N7X19. A crucial premise for co-expression of IL-7 and CCL19 is the capacity to engage other arms of the immune system (e.g. naïve, central memory and regulatory T-cells, B-cells, and dendritic and NK cells) to increase SPEAR T-cell efficacy, which cannot be fully evaluated in the immunodeficient animal models required for these studies. Therefore, a syngeneic model using a surrogate murine T-cell product is required to effectively evaluate of the impact of IL-7 and CCL19 expression in a nonclinical whole-organism setting. In this study, DBA/2CrSlc mice were inoculated with the P815 mouse mastocytoma cell line which is positive for the mouse tumor antigen P1A. Treatments (Table3) were administered by single intravenous injection 14 days after P815 transplantation and 3 days after cyclophosphamide administration. Two mice from each group had serum IFNγ, IL-7 and CCL19 measured at day 6. Table 3: In Vivo Treatment Groups Study groups 3, 4 and 5 had significant decreases in tumor volume by the final day of the study, with 1 mouse each from Groups 2 and 5 and 3 mice in Group 3 fully clearing their tumor. In Groups 2 and 5, one mouse each survived on the final day of the observation period (Figure 9). In Group 4, 2 mice survived, and the survival period was significantly longer than that of Group 1. In Group 3, no dead animals were observed until Day 32, 4 mice survived, and the survival period was significantly longer than that in Group 1. Despite clear evidence of the anti-tumor benefit from the addition of IL-7 and CCL19, neither were detectable in the serum of animals from any group. However, higher values of IFNγ and IL-7 were found in Group 3 in the ELISA analysis of tumor tissues. Whilst anti-tumor effects were observed in all groups with the P1A-TCR_eGFP, the highest anti-tumor effect and greatest overall survival was seen with P1A-TCR_7X19_eGFP, showing a clear benefit to this T-cell therapy by the addition of IL-7 and CCL19 expression.

atgttccatgtttcttttaggtatatctttggacttcctcccctgatccttgttctg ttg M F H V S F R Y I F G L P P L I L V L L Q E I K T C W N K I L M G T K E H - Translated nucleotide sequence (SEQ ID NO: 1) and protein sequence (SEQ ID NO: 2) of IL-7 atgttccacgtgtccttccggtacatcttcggcctgccccccctgatcctggtgctgctg cctgtggccagcagc gactgcgacatcgagggcaaggacggcaagcagtacgagagcgtgctgatggtgtccatc gaccagctgctggac agcatgaaggaaatcggcagcaactgcctgaacaacgagttcaacttcttcaagcggcac atctgcgacgccaac aaagaaggcatgttcctgttcagagccgccagaaagctgcggcagttcctgaagatgaac agcaccggcgacttc gacctgcatctgctgaaagtgtccgagggcaccaccatcctgctgaattgcaccggccaa gtgaagggcagaaag cctgccgccctgggagaagcccagcctaccaagagcctggaagagaacaagtccctgaaa gagcagaagaaactg aacgacctgtgcttcctgaagcggctgctgcaggaaatcaagacctgctggaacaagatc ctgatgggcaccaaa gagcac SEQ ID NO: 3 Codon optimised IL-7 coding sequence MFHVSFRYIFGLPPLILVLLPVASSDCDIEGKDGKQYESVLMVSIDQLLDSMKEIGSNCL NNEFNFFKRHICDAN KEGMFLFRAARKLRQFLKMNSTGDFDLHLLKVSEGTTILLNCTGQVKGRKPAALGEAQPT KSLEENKSLKEQKKL NDLCFLKRLLQEIKTCWNKILMGTKEH SEQ ID NO: 4 IL-7 protein sequence (signal peptide (underlined) 1-25; mature peptide 26- 177) 1 attcccagcc tcacatcact cacaccttgc atttcacccc tgcatcccag tcgccctgca 6 ^{1 gcctcacaca gatcctgcac acacccagac agctggcgct cacacattca ccgttggcct} 121 gcctctgttc accctccatg gccctgctac tggccctcag cctgctggtt ctctggactt 181 ccccagcccc aactctgagt ggcaccaatg atgctgaaga ctgctgcctg tctgtgaccc 241 agaaacccat ccctgggtac atcgtgagga acttccacta ccttctcatc aaggatggct 301 gcagggtgcc tgctgtagtg ttcaccacac tgaggggccg ccagctctgt gcacccccag 361 accagccctg ggtagaacgc atcatccaga gactgcagag gacctcagcc aagatgaagc 421 gccgcagcag ttaacctatg accgtgcaga gggagcccgg agtccgagtc aagcattgtg 481 aattattacc taacctgggg aaccgaggac cagaaggaag gaccaggctt ccagctcctc 541 tgcaccagac ctgaccagcc aggacagggc ctggggtgtg tgtgagtgtg agtgtgagcg 601 agagggtgag tgtggtcaga gtaaagctgc tccaccccca gattgcaatg ctaccaataa 661 agccgcctgg tgtttacaac taa SEQ ID NO: 5 CCL19 mRNA sequence (coding sequence (underlined) 138-434; 5’ (italics) 1-137; 3’ UTR (italics) 435-683) atggctctgc tgctggctct gtctctgctg gtgctgtgga caagccctgc tcctacactg ^{agcggcacca acgatgccga ggattgctgt ctgagcgtga cccagaagcc tattcctggc} tacatcgtgc ggaacttcca ctacctgctg atcaaggacg gctgcagagt gcctgccgtg gtgttcacaa cactgagagg cagacagctg tgcgcccctc ctgatcagcc ttgggtcgag agaatcatcc agagactgca gcggaccagc gccaagatga agagaagaag cagc SEQ ID NO: 6 CCL19 coding sequence (codon optimised) 01 MALLLALSLL VLWTSPAPTL SGTNDAEDCC LSVTQKPIPG YIVRNFHYLL IKDGCRVPAV 61 VFTTLRGRQL CAPPDQPWVE RIIQRLQRTS AKMKRRSS SEQ ID NO: 7 CCL19 protein sequence (signal peptide (underlined) 1-21; mature peptide 22-98) 001 agagacaagc gagcttctgc gtctgactcg cagcttgaga ctggcggagg gaagcccgcc 061 caggctctat aaggagacaa ggttctgagc agacaggcca accggaggac aggattccct 121 ggaggccaca gaggagcacc aaggagaaga tctgcctgtg ggtccccatt gcccagcttt 181 tgcctgcact cttgcctgct gccctgacca gagtcatcat gtcttctgag cagaagagtc 241 agcactgcaa gcctgaggaa ggcgttgagg cccaagaaga ggccctgggc ctggtgggtg 301 cacaggctcc tactactgag gagcaggagg ctgctgtctc ctcctcctct cctctggtcc 361 ctggcaccct ggaggaagtg cctgctgctg agtcagcagg tcctccccag agtcctcagg 421 gagcctctgc cttacccact accatcagct tcacttgctg gaggcaaccc aatgagggtt 481 ccagcagcca agaagaggag gggccaagca cctcgcctga cgcagagtcc ttgttccgag 541 aagcactcag taacaaggtg gatgagttgg ctcattttct gctccgcaag tatcgagcca 601 aggagctggt cacaaaggca gaaatgctgg agagagtcat caaaaattac aagcgctgct 661 ttcctgtgat cttcggcaaa gcctccgagt ccctgaagat gatctttggc attgacgtga 721 aggaagtgga ccccgccagc aacacctaca cccttgtcac ctgcctgggc ctttcctatg 781 atggcctgct gggtaataat cagatctttc ccaagacagg ccttctgata atcgtcctgg 841 gcacaattgc aatggagggc gacagcgcct ctgaggagga aatctgggag gagctgggtg 901 tgatgggggt gtatgatggg agggagcaca ctgtctatgg ggagcccagg aaactgctca 961 cccaagattg ggtgcaggaa aactacctgg agtaccggca ggtacccggc agtaatcctg 1021 cgcgctatga gttcctgtgg ggtccaaggg ctctggctga aaccagctat gtgaaagtcc 1081 tggagcatgt ggtcagggtc aatgcaagag ttcgcattgc ctacccatcc ctgcgtgaag 1141 cagctttgtt agaggaggaa gagggagtct gagcatgagt tgcagccagg gctgtgggga 1201 aggggcaggg ctgggccagt gcatctaaca gccctgtgca gcagcttccc ttgcctcgtg 1261 taacatgagg cccattcttc actctgtttg aagaaaatag tcagtgttct tagtagtggg 1321 tttctatttt gttggatgac ttggagattt atctctgttt ccttttacaa ttgttgaaat 1381 gttcctttta atggatggtt gaattaactt cagcatccaa gtttatgaat cgtagttaac 1 ^{441 gtatattgct gttaatatag tttaggagta agagtcttgt tttttattca gattgggaaa} 1501 tccgttctat tttgtgaatt tgggacataa taacagcagt ggagtaagta tttagaagtg 1561 tgaattcacc gtgaaatagg tgagataaat taaaagatac ttaattcccg ccttatgcct 1621 cagtctattc tgtaaaattt aaaaaatata tatgcatacc tggatttcct tggcttcgtg 1681 aatgtaagag aaattaaatc tgaataaata attctttctg ttaa SEQ ID NO: 8 MAGE A4 mRNA sequence (coding sequence (underlined) 219-1172; 5’ (italics) 1-218; 3’ UTR (italics) 1173-1724) 001 MSSEQKSQHC KPEEGVEAQE EALGLVGAQA PTTEEQEAAV SSSSPLVPGT LEEVPAAESA 061 GPPQSPQGAS ALPTTISFTC WRQPNEGSSS QEEEGPSTSP DAESLFREAL SNKVDELAHF 121 LLRKYRAKEL VTKAEMLERV IKNYKRCFPV IFGKASESLK MIFGIDVKEV DPASNTYTLV 181 TCLGLSYDGL LGNNQIFPKT GLLIIVLGTI AMEGDSASEE EIWEELGVMG VYDGREHTVY 241 GEPRKLLTQD WVQENYLEYR QVPGSNPARY EFLWGPRALA ETSYVKVLEH VVRVNARVRI 301 AYPSLREAAL LEEEEGV SEQ ID NO: 9 MAGE A4 protein sequence (TCR epitope (underlined) 230-239) 01 GVYDGREHTV SEQ ID NO: 10 MAGE A4-derived TCR epitope 0 ^{1 GVYDGEEHSV} SEQ ID NO: 11 MAGE B2-derived TCR epitope MKKHLTTFLVILWLYFYRGNGKNQVEQSPQSLIILEGKNCTLQCNYTVSPFSNLRWYKQD TGRGPVSLTIMTFSE NTKSNGRYTATLDADTKQSSLHITASQLSDSASYICVVSGGTDSWGKLQF SEQ ID NO: 12 parental TCR alpha variable chain protein sequence (signal underlined) MASLLFFCGAFYLLGTGSMDADVTQTPRNRITKTGKRIMLECSQTKGHDRMYWYRQDPGL GLRLIYYSFDVKDIN KGEISDGYSVSRQAQAKFSLSLESAIPNQTALYFCATSGQGAYNEQFF SEQ ID NO: 13 parental TCR beta variable chain protein sequence(signal underlined) KNQVEQSPQSLIILEGKNCTLQCNYTVSPFSNLRWYKQDTGRGPVSLTILTFSENTKSNG RYTATLDADTKQSSL HITASQLSDSASYICVVSGGTDSWGKLQF SEQ ID NO: 14 TCR alpha chain variable domain (CDRs bold underlined, no signal peptide) DVTQTPRNRITKTGKRIMLECSQTKGHDRMYWYRQDPGLGLRLIYYSFDVKDINKGEISD GYSVSRQAQAKFSLS LESAIPNQTALYFCATSGQGAYEEQFF SEQ ID NO: 15 TCR beta chain variable domain (CDRs bold underlined, no signal peptide) MKKHLTTFLVILWLYFYRGNGKNQVEQSPQSLIILEGKNCTLQCNYTVSPFSNLRWYKQD TGRGPVSLTILTFSE NTKSNGRYTATLDADTKQSSLHITASQLSDSASYICVVSGGTDSWGKLQFGAGTQVVVTP DIQNPDPAVYQLRDS KSSDKSVCLFTDFDSQTNVSQSKDSDVYITDKTVLDMRSMDFKSNSAVAWSNKSDFACAN AFNNSIIPEDTFFPS PESSCDVKLVEKSFETDTNLNFQNLSVIGFRILLLKVAGFNLLMTLRLWSS SEQ ID NO: 16 TCR alpha chain (CDRs bold underlined, signal sequence italic underlined) MASLLFFCGAFYLLGTGSMDADVTQTPRNRITKTGKRIMLECSQTKGHDRMYWYRQDPGL GLRLIYYSFDVKDIN KGEISDGYSVSRQAQAKFSLSLESAIPNQTALYFCATSGQGAYEEQFFGPGTRLTVLEDL KNVFPPEVAVFEPSE AEISHTQKATLVCLATGFYPDHVELSWWVNGKEVHSGVSTDPQPLKEQPALNDSRYCLSS RLRVSATFWQNPRNH FRCQVQFYGLSENDEWTQDRAKPVTQIVSAEAWGRADCGFTSESYQQGVLSATILYEILL GKATLYAVLVSALVL MAMVKRKDSRG SEQ ID NO: 17 TCR beta chain (CDRs bold underlined, signal sequence italic underlined) MKKHLTTFLVILWLYFYRGNGKNQVEQSPQSLIILEGKNCTLQCNYTVSPFSNLRWYKQD TGRGPVSLTILTFSE NTKSNGRYTATLDADTKQSSLHITASQLSDSASYICVVSGGTDSWGKLQFGAGTQVVVTP DIQNPDPAVYQLRDS KSSDKSVCLFTDFDSQTNVSQSKDSDVYITDKTVLDMRSMDFKSNSAVAWSNKSDFACAN AFNNSIIPEDTFFPS PESSCDVKLVEKSFETDTNLNFQNLSVIGFRILLLKVAGFNLLMTLRLWSSGSRAKRSGS GATNFSLLKQAGDVE ENPGPRMASLLFFCGAFYLLGTGSMDADVTQTPRNRITKTGKRIMLECSQTKGHDRMYWY RQDPGLGLRLIYYSF DVKDINKGEISDGYSVSRQAQAKFSLSLESAIPNQTALYFCATSGQGAYEEQFFGPGTRL TVLEDLKNVFPPEVA VFEPSEAEISHTQKATLVCLATGFYPDHVELSWWVNGKEVHSGVSTDPQPLKEQPALNDS RYCLSSRLRVSATFW QNPRNHFRCQVQFYGLSENDEWTQDRAKPVTQIVSAEAWGRADCGFTSESYQQGVLSATI LYEILLGKATLYAVL VSALVLMAMVKRKDSRG SEQ ID NO: 18 MAGEA4 TCR alpha and beta chains linked by FuP2A (alpha and beta variable domains underlined, P2A skip peptide double underlined) ATGAAGAAGCACCTGACCACCTTTCTCGTGATCCTGTGGCTGTACTTCTACCGGGGCAAC GGCAAGAACCAGGTG GAACAGAGCCCCCAGAGCCTGATCATCCTGGAAGGCAAGAACTGCACCCTGCAGTGCAAC TACACCGTGTCCCCC TTCAGCAACCTGCGGTGGTACAAGCAGGACACCGGCAGAGGCCCTGTGTCCCTGACCATC CTGACCTTCAGCGAG AACACCAAGAGCAACGGCCGGTACACCGCCACCCTGGACGCCGATACAAAGCAGAGCAGC CTGCACATCACCGCC AGCCAGCTGAGCGATAGCGCCAGCTACATCTGCGTGGTGTCCGGCGGCACAGACAGCTGG GGCAAGCTGCAGTTT GGCGCCGGAACACAGGTGGTCGTGACCCCCGACATCCAGAACCCTGACCCTGCCGTGTAC CAGCTGCGGGACAGC AAGAGCAGCGACAAGAGCGTGTGCCTGTTCACCGACTTCGACAGCCAGACCAACGTGTCC CAGAGCAAGGACAGC GACGTGTACATCACCGACAAGACCGTGCTGGACATGCGGAGCATGGACTTCAAGAGCAAT AGCGCCGTGGCCTGG TCCAACAAGAGCGACTTCGCCTGCGCCAACGCCTTCAACAACAGCATTATCCCCGAGGAC ACATTCTTCCCAAGC CCCGAGAGCAGCTGCGACGTCAAGCTGGTGGAAAAGAGCTTCGAGACAGACACCAACCTG AACTTCCAGAACCTG AGCGTGATCGGCTTCAGAATCCTGCTGCTGAAGGTGGCCGGCTTCAACCTGCTGATGACC CTGAGACTGTGGTCC AGCGGCAGCCGGGCCAAGAGATCTGGATCCGGCGCTACCAACTTTAGCCTGCTGAAGCAG GCCGGGGACGTGGAA ^{GAAAACCCTGGCCCTAGGATGGCCAGCCTGCTGTTCTTCTGCGGCGCCTTCTACC TGCTGGGCACCGGCTCTATG} GATGCCGACGTGACCCAGACCCCCCGGAACAGAATCACCAAGACCGGCAAGCGGATCATG CTGGAATGCTCCCAG ACCAAGGGCCACGACCGGATGTACTGGTACAGACAGGACCCTGGCCTGGGCCTGCGGCTG ATCTACTACAGCTTC GACGTGAAGGACATCAACAAGGGCGAGATCAGCGACGGCTACAGCGTGTCCAGACAGGCT CAGGCCAAGTTCAGC CTGTCCCTGGAAAGCGCCATCCCCAACCAGACCGCCCTGTACTTTTGTGCCACAAGCGGC CAGGGCGCCTACGAG ^{GAGCAGTTCTTTGGCCCTGGCACCCGGCTGACAGTGCTGGAAGATCTGAAGAACG TGTTCCCCCCAGAGGTGGCC} GTGTTCGAGCCTTCTGAGGCCGAAATCAGCCACACCCAGAAAGCCACACTCGTGTGTCTG GCCACCGGCTTCTAC CCCGACCACGTGGAACTGTCTTGGTGGGTCAACGGCAAAGAGGTGCACAGCGGCGTGTCC ACCGATCCCCAGCCT CTGAAAGAACAGCCCGCCCTGAACGACAGCCGGTACTGCCTGAGCAGCAGACTGAGAGTG TCCGCCACCTTCTGG CAGAACCCCAGAAACCACTTCAGATGCCAGGTGCAGTTTTACGGCCTGAGCGAGAACGAC GAGTGGACCCAGGAC AGAGCCAAGCCCGTGACACAGATCGTGTCTGCCGAAGCTTGGGGGCGCGCCGATTGTGGC TTTACCAGCGAGAGC TACCAGCAGGGCGTGCTGAGCGCCACCATCCTGTACGAGATCCTGCTGGGAAAGGCCACA CTGTACGCCGTGCTG GTGTCTGCCCTGGTGCTGATGGCCATGGTCAAGCGGAAGGACAGCCGGGGC SEQ ID NO: 19 Nucleotide sequence encoding MAGEA4 TCR alpha and beta chains linked by FuP2A GGAGGAAAAACTGTTTCATACAGAAGGCGT SEQ ID NO: 20 human IL2 promoter NFAT TRE TAGGCGTGTACGGTGGGAGGCCTATATAAGCAGAGCTCGTTTAGTGAACCGTCAGATCGC CTGGAGAC GCCATCCACGCTGTTTTGACCTCCATAGAAGACACCGGGACCGATCCAGCCTCTCGACAT TCGTTGGA TCSEQ ID NO: 21 minimal CMV promoter ACCGGTTCAATTGCCGACCCCTCCCCCCAACTTCTCGGGGACTGTGGGCGATGTGCGCTC TGCCCACTGACGGGC ACCGGAGCCTCACGATGCATGATATCGGCCTAACTGGCCGGTACCTGAGCTCGCTAGCGG AGGAAAAACTGTTTC ATACAGAAGGCGTGGAGGAAAAACTGTTTCATACAGAAGGCGTGGAGGAAAAACTGTTTC ATACAGAAGGCGTga cgtcTAGGCGTGTACGGTGGGAGGCCTATATAAGCAGAGCTCGTTTAGTGAACCGTCAGA TCGCCTGGAGACGCC ATCCACGCTGTTTTGACCTCCATAGAAGACACCGGGACCGATCCAGCCTCTCGACATTCG TTGGATCCATATGGC CGCCACCATGTTCCATGTTTCTTTTAGGTATATCTTTGGACTTCCTCCCCTGATCCTTGT TCTGTTGCCAGTAGC ATCATCTGATTGTGATATTGAAGGTAAAGATGGCAAACAATATGAGAGTGTTCTAATGGT CAGCATCGATCAATT ATTGGACAGCATGAAAGAAATTGGTAGCAATTGCCTGAATAATGAATTTAACTTTTTTAA AAGACATATCTGTGA TGCTAATAAGGAAGGTATGTTTTTATTCCGTGCTGCTCGCAAGTTGAGGCAATTTCTTAA AATGAATAGCACTGG TGATTTTGATCTCCACTTATTAAAAGTTTCAGAAGGCACAACAATACTGTTGAACTGCAC TGGCCAGGTTAAAGG AAGAAAACCAGCTGCCCTGGGTGAAGCCCAACCAACAAAGAGTTTGGAAGAAAATAAATC TTTAAAGGAACAGAA AAAACTGAATGACTTGTGTTTCCTAAAGAGACTATTACAAGAGATAAAAACTTGTTGGAA TAAAATTTTGATGGG CACTAAAGAACACTGACTCGAGAACTTGTTTATTGCAGCTTATAATGGTTACAAATAAAG CAATAGCATCACAAA TTTCACAAATAAAGCATTTTTTTCACTGCATTCTAGTTGTGGTTTGTCCAAACTCATCAA TGTATCTTAACGCGT SEQ ID NO: 22 Nucleotide sequence of an NFAT IL-7 inducible cassette. Key: Full underline = Tandem repeats of the human IL2 promoter NFAT TRE (GGAGGAAAAACTGTTTCATACAGAAGGCGT). Dashed underline = Minimal CMV promoter. Italics = Kozak sequence (GCCGCCACCATG) Double underline = parental IL-7 coding sequence. Dotted underline = SV40 polyadenylation signal. ACCGGTTCAATTGCCGACCCCTCCCCCCAACTTCTCGGGGACTGTGGGCGATGTGCGCTC TGCCCACTGACGGGC ACCGGAGCCTCACGATGCATGATATCGGCCTAACTGGCCGGTACCTGAGCTCGCTAGCGG AGGAAAAACTGTTTC ATACAGAAGGCGTGGAGGAAAAACTGTTTCATACAGAAGGCGTGGAGGAAAAACTGTTTC ATACAGAAGGCGTga cgtcTAGGCGTGTACGGTGGGAGGCCTATATAAGCAGAGCTCGTTTAGTGAACCGTCAGA TCGCCTGGAGACGCC ATCCACGCTGTTTTGACCTCCATAGAAGACACCGGGACCGATCCAGCCTCTCGACATTCG TTGGATCCATATGGC CGCCACCATGTTCCACGTGTCCTTCCGGTACATCTTCGGCCTGCCCCCCCTGATCCTGGT GCTGCTGCCTGTGGC CAGCAGCGACTGCGACATCGAGGGCAAGGACGGCAAGCAGTACGAGAGCGTGCTGATGGT GTCCATCGACCAGCT GCTGGACAGCATGAAGGAAATCGGCAGCAACTGCCTGAACAACGAGTTCAACTTCTTCAA GCGGCACATCTGCGA CGCCAACAAAGAAGGCATGTTCCTGTTCAGAGCCGCCAGAAAGCTGCGGCAGTTCCTGAA GATGAACAGCACCGG CGACTTCGACCTGCATCTGCTGAAAGTGTCCGAGGGCACCACCATCCTGCTGAATTGCAC CGGCCAAGTGAAGGG CAGAAAGCCTGCCGCCCTGGGAGAAGCCCAGCCTACCAAGAGCCTGGAAGAGAACAAGTC CCTGAAAGAGCAGAA GAAACTGAACGACCTGTGCTTCCTGAAGCGGCTGCTGCAGGAAATCAAGACCTGCTGGAA CAAGATCCTGATGGG CACCAAAGAGAACTTGTTTATTGCAGCTTATAATGGTTACAAATAAAGCAATAGCATCAC AAATTTCACAAATAA AGCATTTTTTTCACTGCATTCTAGTTGTGGTTTGTCCAAACTCATCAATGTATCTTAACG CGT SEQ ID NO: 23 Nucleotide sequence of an NFAT IL-7 inducible cassette. Key: Full underline = Tandem repeats of the human IL2 promoter NFAT TRE (GGAGGAAAAACTGTTTCATACAGAAGGCGT). Dashed underline = Minimal CMV promoter. Italics = Kozak sequence (GCCGCCACCATG) Double underline = codon optimised IL-7 coding sequence. Dotted underline = SV40 polyadenylation signal. ATGAAGAAGCACCTGACCACCTTTCTCGTGATCCTGTGGCTGTACTTCTACCGGGGCAAC GGCAAGAAC CAGGTGGAACAGAGCCCCCAGAGCCTGATCATCCTGGAAGGCAAGAACTGCACCCTGCAG TGCAACTAC ACCGTGTCCCCCTTCAGCAACCTGCGGTGGTACAAGCAGGACACCGGCAGAGGCCCTGTG TCCCTGACC ATCCTGACCTTCAGCGAGAACACCAAGAGCAACGGCCGGTACACCGCCACCCTGGACGCC GATACAAAG CAGAGCAGCCTGCACATCACCGCCAGCCAGCTGAGCGATAGCGCCAGCTACATCTGCGTG GTGTCCGGC GGCACAGACAGCTGGGGCAAGCTGCAGTTTGGCGCCGGAACACAGGTGGTCGTGACCCCC GACATCCAG AACCCTGACCCTGCCGTGTACCAGCTGCGGGACAGCAAGAGCAGCGACAAGAGCGTGTGC CTGTTCACC GACTTCGACAGCCAGACCAACGTGTCCCAGAGCAAGGACAGCGACGTGTACATCACCGAC AAGACCGTG CTGGACATGCGGAGCATGGACTTCAAGAGCAATAGCGCCGTGGCCTGGTCCAACAAGAGC GACTTCGCC TGCGCCAACGCCTTCAACAACAGCATTATCCCCGAGGACACATTCTTCCCAAGCCCCGAG AGCAGCTGC GACGTCAAGCTGGTGGAAAAGAGCTTCGAGACAGACACCAACCTGAACTTCCAGAACCTG AGCGTGATC GGCTTCAGAATCCTGCTGCTGAAGGTGGCCGGCTTCAACCTGCTGATGACCCTGAGACTG TGGTCCAGC GGCAGCCGGGCCAAGAGATCTGGATCCGGCGCTACCAACTTTAGCCTGCTGAAGCAGGCC GGGGACGTG GAAGAAAACCCTGGCCCTAGGATGGCCAGCCTGCTGTTCTTCTGCGGCGCCTTCTACCTG CTGGGCACC GGCTCTATGGATGCCGACGTGACCCAGACCCCCCGGAACAGAATCACCAAGACCGGCAAG CGGATCATG C ^{TGGAATGCTCCCAGACCAAGGGCCACGACCGGATGTACTGGTACAGACAGGACCC TGGCCTGGGCCTG} CGGCTGATCTACTACAGCTTCGACGTGAAGGACATCAACAAGGGCGAGATCAGCGACGGC TACAGCGTG TCCAGACAGGCTCAGGCCAAGTTCAGCCTGTCCCTGGAAAGCGCCATCCCCAACCAGACC GCCCTGTAC TTTTGTGCCACAAGCGGCCAGGGCGCCTACGAGGAGCAGTTCTTTGGCCCTGGCACCCGG CTGACAGTG CTGGAAGATCTGAAGAACGTGTTCCCCCCAGAGGTGGCCGTGTTCGAGCCTTCTGAGGCC GAAATCAGC CACACCCAGAAAGCCACACTCGTGTGTCTGGCCACCGGCTTCTACCCCGACCACGTGGAA CTGTCTTGG TGGGTCAACGGCAAAGAGGTGCACAGCGGCGTGTCCACCGATCCCCAGCCTCTGAAAGAA CAGCCCGCC CTGAACGACAGCCGGTACTGCCTGAGCAGCAGACTGAGAGTGTCCGCCACCTTCTGGCAG AACCCCAGA AACCACTTCAGATGCCAGGTGCAGTTTTACGGCCTGAGCGAGAACGACGAGTGGACCCAG GACAGAGCC AAGCCCGTGACACAGATCGTGTCTGCCGAAGCTTGGGGGCGCGCCGATTGTGGCTTTACC AGCGAGAGC TACCAGCAGGGCGTGCTGAGCGCCACCATCCTGTACGAGATCCTGCTGGGAAAGGCCACA CTGTACGCC GTGCTGGTGTCTGCCCTGGTGCTGATGGCCATGGTCAAGCGGAAGGACAGCCGGGGCGGA AGCCGTGCA AAGAGAAGCggcggcggagagggcagaggaagtcttctaacatgcggtgacgtggaggag aatcccggc cctATGGCTCTGCTGCTGGCTCTGTCTCTGCTGGTGCTGTGGACAAGCCCTGCTCCTACA CTGAGCGGC ACCAACGATGCCGAGGATTGCTGTCTGAGCGTGACCCAGAAGCCTATTCCTGGCTACATC GTGCGGAAC T ^{TCCACTACCTGCTGATCAAGGACGGCTGCAGAGTGCCTGCCGTGGTGTTCACAAC ACTGAGAGGCAGA} CAGCTGTGCGCCCCTCCTGATCAGCCTTGGGTCGAGAGAATCATCCAGAGACTGCAGCGG ACCAGCGCC AAGATGAAGAGAAGAAGCAGCggatcccgggccaagcggagcggatctggcgcccctgtg aagcagacc ctgaatttcgacctgctgaagctggccggcgacgtggaaagcaaccctggccccATGTTC CACGTGTCC TTCCGGTACATCTTCGGCCTGCCCCCCCTGATCCTGGTGCTGCTGCCTGTGGCCAGCAGC GACTGCGAC ATCGAGGGCAAGGACGGCAAGCAGTACGAGAGCGTGCTGATGGTGTCCATCGACCAGCTG CTGGACAGC ATGAAGGAAATCGGCAGCAACTGCCTGAACAACGAGTTCAACTTCTTCAAGCGGCACATC TGCGACGCC AACAAAGAAGGCATGTTCCTGTTCAGAGCCGCCAGAAAGCTGCGGCAGTTCCTGAAGATG AACAGCACC GGCGACTTCGACCTGCATCTGCTGAAAGTGTCCGAGGGCACCACCATCCTGCTGAATTGC ACCGGCCAA GTGAAGGGCAGAAAGCCTGCCGCCCTGGGAGAAGCCCAGCCTACCAAGAGCCTGGAAGAG AACAAGTCC CTGAAAGAGCAGAAGAAACTGAACGACCTGTGCTTCCTGAAGCGGCTGCTGCAGGAAATC AAGACCTGC TGGAACAAGATCCTGATGGGCACCAAAGAGCACTAA SEQ ID NO: 24 Nucleotide sequence of the construct c1032alpha_FuP2A_c1032beta_FuT2A_CCL19_FuF2A_IL7 (from initiating methionine until stop codon included). TCR plain; IL-7 underlined; CCL19 italics