Compensatory IFNγ drives increased CXCR3 ligands in the absence of IFNAR signaling. (A) NES plot of hallmark type I and II interferon, and inflammation responses. Data are generated as indicated in Fig. 3. NES represents the fold change of all cells analyzed in each condition, relative to expression in all other conditions. (B) Concentration of IFNγ in lysates of lymph nodes at d8 following acute LCMV infection. Each dot represents a single mouse sample. Data are the mean ± SEM. Statistical differences were analyzed using one-way ANOVA tests. (C and D) Expression of Cxcl9-RFP and Cxcl10-BFP in cDC1, cDC2, and moDC populations from REX3 hosts crossed to indicated IFN-deficient mice at d8 of acute LCMV infection. 2xIFN^−/− = Ifnar^−/−Ifng^−/−. Data are representative of three individual repeats with at least three mice in each group in each experiment. (C) Representative flow cytometry plots. (D) Graphs summarizing graded frequencies of Cxcl9-RFP and Cxcl10-BFP expression from C. Graded expression summarized in key. (E) LSFM micrographs of intact wild-type, Ifnar^−/−, Ifng^−/−, or 2xIFN^−/− mouse REX3 lymph nodes. Images are 200-µm longitudinal slices through the lymph node center. Scale bars represent 100 µm. Images show Cxcl9-RFP (magenta), Cxcl10-BFP (cyan), B220 (B cells; yellow), and CD31 (vessels; white). Images are representative of three individual experiments with at least three mice in each group in each experiment. **P < 0.01. Fig. S4 shows additional supporting data.