Fig. 8: GPR182 ablation sensitizes tumors to immunotherapy.

a, b WT and GPR182−/− mice were inoculated with 50,000 YUMM1.7 tumor cells and treated with ICB (anti-CTLA-4 and anti-PD1) or vehicle control (arrows indicate ICB treatment). Tumor growth (a) and Kaplan–Meier survival (b) curves for YUMM1.7 were indicated. WT, n = 10; WT (ICB), n = 10; GPR182−/−, n = 8; GPR182−/− (ICB), n = 10. c Tumor growth curves for WT and GPR182−/− mice inoculated with B16 tumors and treated with anti-PD1 or control after the establishment of tumors (arrows indicate anti-PD1 therapy). n = 10 per group. d WT and GPR182−/− mice were s.c. inoculated with 500,000 B16-OVA tumor cells; On day 6, half of the mice received i.v. transfer of activated OT-1 cells. Tumor growth curves for B16-OVA were followed daily. n = 10 per group. Representative data from two independent experiments. e A scheme describes how GPR182 functions as a chemokine scavenger to suppress antitumor immunity. P-values for growth curves from two-way ANOVA test (a, c, d). P-values for tumor mass from student’s t-test. P-values for Kaplan–Meier curves from log-rank test, two-sided (b). Error bars represent SEM.