Figure 5: STING agonism increases type I IFN signaling and promotes antitumor immunity.
KitV558Δ/+ mice treated with vehicle (7.5% NaCO2) or DMXAA (200 μg/mouse) for 3 weeks. Unpaired two-sample t-test of DMXAA treatment performed against vehicle controls. Data represent mean ± SEM, * p-value < 0.05, ** p-value <0.01, *** p-value <0.001. N=3–5 mice/group, repeated twice. (A) Tumor weights and representative tumor photos shown. (B) RT-PCR of tumor Ifnb1 expression in DMXAA-treated mice relative to vehicle. (C) Immunoblot of KIT and STAT1 signaling in tumors from (A). (D) MHC class I expression on KIT+ tumor cells from (A) by MFI using flow cytometry analysis. Pooled between two experiments and expressed as ratio to the mean MHC class I MFI of the control group. (E) Flow cytometry frequency of macrophages (CD11b+F480+) and DCs (CD11c+MHCII+) as percentage of immune cells. MHC class II expression (MHC II) on macrophages (F480+) also measured by MFI. (F) Flow cytometry frequency of intratumoral CD8+ T cells expressed as percentage of immune cells. Intratumoral CD8+ T cells analyzed for PD1 and CD103 expression. (G) Gene expression of Cxcl9, Cxcl10, and Tnf in tumors from (A) relative to vehicle treatment. (H) Tumor weights of KitV558Δ/+ mice treated with vehicle, DMXAA or DMXAA and anti-CD8 (200μg/mouse) for 3 weeks. N=4 mice/group.