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. 2022 Dec 12;7(1):24–37. doi: 10.1038/s41551-022-00969-0

Fig. 4. Signal enhancement improved the accumulation, persistency, and effector function of iCAR-TCTL.

Fig. 4

a, Schematic presentation of the mbIL-15 constructs used in this study. Each construct was inserted under the retroviral long terminal repeat (LTR) promoter. tLNGFR, truncated form of low-affinity nerve growth factor receptor and marker of transduced mbIL15. b, Proliferation of iCAR-TCTL and pCAR-TCTL in the presence or absence of additional IL-15 or transgene modification of mbIL-15 (n = 3, mean ± s.e.m.). Proliferation was determined 72 h after co-culturing with irradiated SK-Hep-GPC3 using a standard [3H]-thymidine incorporation assay. c, Therapeutic efficacy of iCAR-TCTL and iCAR-TCTL mbIL-15 with a subcutaneous liver cancer model. The treatment schedule of the liver cancer subcutaneous xenograft model. NSG mice were injected intraperitoneally (i.p.) with 2 × 105 JHH7 cells 3 days before treatment. Three days after the liver cancer inoculation, 1 × 107 iCAR-TCTL or iCAR-TCTL-mbIL15tg were administered intravenously. d, In vivo bioluminescence imaging of the injected T cells in NSG mice. e, Total flux (photons s−1) of the injected iCAR-T cells in the JHH7 tumour was quantified at the indicated timepoints (n = 5 of each group). Two-sided Student’s t-test. f, Volume of inoculated JHH7 at the indicated timepoints in individual mice treated with the indicated test cells. Mean tumour size ± s.e.m. (n = 5 of each group). Two-way ANOVA.

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