Fig. 2

IL-21 promoted activation-induced proliferation and improved in vivo anti-HCC function of TCR-T. a The process of generating human TCR-T and IL-21 stimulation was shown. The cell growth of TCR-T during expanding was monitored. Mock transduced T cells had undergone the same expanding procedure without lv transduction. b, c The proliferating fold change of CD8⁺ and CD4⁺ TCR-T after CD3/CD28 activation in the presence of IL-2 (10 ng/ml) or IL-2 (10 ng/ml) and IL-21 (20 ng/ml) was shown respectively (n = 3). d TCR-T were labeled by CFSE, cultured with HepG2 for 96 h in the presence of IL-2 or IL-2 and IL-21 and analyzed by flow cytometry. The percentage of divided cells in the CD8⁺ subset was shown (n = 3). The brown peak indicated the first proliferating generation, the red indicated the second, the green indicated the third and the blue indicated the fourth. e The fold change of CD8⁺ TCR-T percentage in total T cells during the repetitive coculture assay was shown (n = 3). f Schematics of subcutaneous HepG2 model establishment and adoptive transfer process in NPG mice. g The mice tumor volume in each group after HepG2 implantation and mock-transduced T or TCR-T cell transfer was shown (n = 5). h The TCR-T percentage in total lymphocytes (mice and human lymphocytes) in mice peripheral blood 1, 7 and 14 days after TCR-T transfer was shown (n = 5). i Tumors were isolated at the end of the experiment from tumor-bearing mice receiving mock-transduced T or TCR-T treatment with or without IL-21 and the weight of isolated tumors was shown (n = 5). Data were shown as mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, NS not significant, ACT adoptive cell transfer