Loss of Trex1 in dMMR tumor provokes CD8 ⁺ T cell–mediated antitumor immunity. (A) 4T1 and 4T1-Mlh1^−/− (day 75) cells (n = 3/group) were collected for DNase mRNA detection by RT-qPCR. (B) BALB/c mice (n = 4) were transplanted s.c. with 5 × 10⁵ 4T1, Trex1^−/−, Mlh1^−/− (day 70), or Mlh1^−/−Trex1^−/− (day 70) cells. (C) 615 mice (n = 5) were transplanted s.c. with 1 × 10⁷ MFC, Trex1^−/−, Mlh1^−/− (day 78), or Mlh1^−/−Trex1^−/− (day 78) cells. (D) C57BL/6 mice (n = 5) were transplanted s.c. with 2 × 10⁶ MC38 or MC38-Trex1^−/− cells. (E) C57BL/6 mice and Rag1^−/− mice (n = 5) were transplanted s.c. with 2 × 10⁶ MC38-Trex1^−/− cells. (F) C57BL6/J mice were transplanted s.c. with 2 × 10⁶ MC38 WT or MC38-Trex1^−/− cells and treated with IgG, anti-CD4+anti-NK1.1, anti-CD4+anti-CD8, or anti-CD8 antibodies (200 μg/mouse). Tumor growth is shown. (G–J) C57BL/6 mice (n = 5) were transplanted s.c. with 1 × 10⁷ MC38 WT or MC38-Trex1^−/− cells. 15 days later, tumor tissues were collected and analyzed by flow cytometry. The percentage of CD45⁺ cell in tumor (G), CD8⁺ T cell in CD45⁺ immune cells (H), CD8⁺ T cell and CD4⁺ T cell in tumor (I), or MC38 antigen-specific CD8⁺ T cell (KSP⁺CD8⁺ T cell) in tumor tissue (J) is shown. Data indicate mean ± SEM and are representative of two (A–J) independent experiments. The statistical analysis was performed by two-way ANOVA in B–F and unpaired Student’s two-tailed t test in A and G–J. NS, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.