Extended Data Fig. 6: FcγR engagement drives a robust activation of type-I IFN signaling.
(a) Comparison of the fractions of the indicated cell populations in individual mice in each genotype and treatment group. n = 6, 4, and 3 biologically independent samples for each of Ctrl, m1 and m2a in WT, FCGR KO and IFNAR KO groups respectively, were used for statistical analysis. (b) Scatterplot comparing anti-CTLA-4 m2a WT (Y) vs. anti-CTLA-4 m2a FCGR KO (X) gene expression changes in BMDM cells. Leading DEGs are annotated. (c) Scatterplot comparing anti-CTLA-4 m2a WT (Y) vs. anti-CTLA-4 m2a IFNAR KO (X) gene expression changes in BMDM cells. Leading DEGs are annotated. (d) Scatterplot comparing anti-CTLA-4 m2a FCGR KO (Y) vs. anti-CTLA-4 m2a IFNAR KO (X) gene expression changes in BMDM cells. Leading DEGs are annotated. (e) Percent of proliferating T cells and interferon gamma secretion in idle T cells, activated T cells, and activated T cells co-cultured with Cd11b+ cells purified from MCA-205 tumors treated with anti-CTLA-4 m2a in WT or IFNAR KO mice. n = 4 biologically independent samples for each group were used for statistical analysis. In (a), bars represent mean ± SE of mice per treatment arm. Two-way ANOVA (fraction ~ treatment * batch) was used. Differential gene expression is estimated using two-sided Wilcoxon rank-sum test, Benjamini-Hochberg adjusted p-value < 0.05, FC > 1.25.
