IRF7 regulates translation and metabolism during B cell activation. (A) Ingenuity pathway analysis of differentially expressed genes within the pre-GC clusters of the scRNAseq data from FcγRIIB^−/− and FcγRIIB^−/−IRF7^−/− mice. (B) The heatmaps of upregulated and downregulated genes linked to EIF2 signaling and OXPHOS between FcγRIIB^−/− and FcγRIIB^−/−IRF7^−/− pre-GC clusters. (C) The pie chart showing the genomic locations of IRF7 peaks from ChIP-seq analysis of antigen-experienced IgD⁻ B cells from FcγRIIB^−/− mice. (D) The volcano plot of IRF7 target genes identified by ChIP-seq analysis, which are upregulated and downregulated between FcγRIIB^−/− and FcγRIIB^−/−IRF7^−/− B cells in scRNAseq analysis. (E) Representative IRF7 peaks in the promoters of several ribosomal protein genes. (F and G) Extracellular flux analysis showing OXPHOS and glycolysis of FcyRIIB^−/−IRF7^−/− and FcyRIIB^−/− B cells, including basal respiration and non-mitochondrial OCR. (H) Translation analysis in total and spontaneously activated B cells from FcγRIIB^−/− and FcγRIIB^−/−IRF7^−/− mice. (I) Analysis of translation in TLR7-activated B cells from FcγRIIB^−/− and FcγRIIB^−/−IRF7^−/− mice by flow cytometry. Data in A–E represent four mice. Each symbol in F–I represents an individual mouse (n = 3–6 mice per group), and data are presented as means ± SEM. Data in F–I represent two to four experiments. P values were calculated via an unpaired Student’s t test (F and G) or two-way ANOVA with Dunn–Sidak correction (H and I) (not significant, NS, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001).