Fig. 8: T-αFGL2-induced CD69⁺CD8⁺T_M cells were associated with CXCL9/10-CXCR3 axis.

a Expression levels of CCR2, CSF1R, CXCR2, CXCR3, and CX3CR1 on CD69⁺CD8⁺T_M cell populations; CyTOF analysis was conducted on day 2–4 after the second T cell treatment. (n = 5 mice per group; data represent mean ± SD), p value from two-tailed t-test, FDR false discovery rate. b Representative flow cytometry plots and graphs showing that T-αFGL2 treatment increased the proportion of CXCR3⁺CD69⁺CD8⁺T cells among total CD8⁺T cells in glioma-bearing brains (n = 5 mice/group; data represent mean ± SD), two-tailed t-test. c Kaplan–Meier survival curves of GL261-bearing WT mice and CXCR3^−/− mice treated with T-Ctr or T-αFGL2 (n = 5 mice/group), log-rank test. d Number of CD69⁺CD8⁺T_M cells per GL261-bearing brain on day 5–7 after the second T cell infusion (n = 5 per group; data represent mean ± SEM), one-way ANOVA with Dunnett’s test for comparing multiple treatments. e, f Quantitative analysis of CXCL9 and CXCL10 protein levels in DBT tumors from mice 4–6 days after the second infusion of T-Ctr or T-αFGL2 cells (n = 5 per group; data represent mean ± SEM), two-way t-test. g Percentages of CD69⁺ cells among CD44⁺CD8⁺T cells (n = 5 per group; data represent mean ± SEM), one-way ANOVA with Dunnett’s test for comparing multiple treatments. NS not significant. h Schematic illustration of cellular and molecular events underlying T-αFGL2–induced tumor-specific brain-resident CD8⁺T_RM cells. T-αFGL2 cells block FGL2 in the tumor microenvironment, resulting in CXCL9/10 induction. The CXCL9/10-CXCR3 engagement boosts recruitment of CXCR3⁺CD69⁺CD8⁺T cells, which are candidate tumor-specific brain-resident CD8⁺T_RM cells.