AIM2-deficient DC vaccination facilitates tumor antigen–specific CD8+ T cell infiltration into the tumor via IFNAR signaling and CXCL10 production.(A) IFN-β or CXCL10 in the supernatants of indicated BMDCs stimulated with 0, 0.1, or 1 µg/ml B16F10 DNA for 4 (IFN-β) or 10 h (CXCL10; n = 3). (B–D) B16F10 mice were treated with ACT + WT, Aim2−/−, Aim2−/−Ifnar−/−, or Aim2−/−Cxcl10−/− DC-gp100. On day 20 after PMELs transfer, tissues were harvested (n = 10 or 11). (B) Tumor growth over time. (C and D) Flow cytometry analysis of TILs. (C) The numbers of PMELs, CD8+ T cells, and CD4+ T cells among 104 live singlet cells, percentages of FoxP3+ cells in CD4+ T cells, and PMEL/T reg cell ratio. (D) The percentages of IFN-γ+ and TNF-α+ in CD8+ T cells. (E–G) Similar analysis as in B–D was performed on B16F10 mice treated by ACT with WT, Aim2−/−Cxcl10−/−, or Cxcl10−/− DC-gp100 (n = 8 or 9). Data are shown as mean ± SEM and are pooled from three independent experiments (A–G). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; two-way ANOVA with Tukey’s multiple-comparisons test (B and E) or one-way ANOVA with Dunnett’s (A) or Tukey’s (C, D, and F) multiple-comparisons test.