Figure 3.

Type I IFN signaling increases intestinal permeability and immune cell recruitment genes while down-regulating tight junction–related genes in IECs from LCMV-Cl13–infected mice. See also Fig. S3, Table S6, Table S7, Table S8, and Table S9.C57BL/6 mice were infected with LCMV Cl13 or left uninfected (Un) and injected with isotype (IgG1) or anti-IFNAR-1 Ab (αIFNAR) i.p. and analyzed at day 9 p.i. (A) In vivo intestinal permeability to FD4. (B–E) RNA sequencing was performed in IECs. (B) PCA plots showing individual samples from IgG1- versus αIFNAR-treated Cl13-infected mice. (C and D) Venn diagram overlapping pathways (C) or DEGs (D) from Cl13 versus ARM (data from Fig. 2) and Cl13-infected plus IgG1 versus αIFNAR treatment comparisons. (E) DEGs in IEC transcriptomes from IgG1- versus αIFNAR-treated Cl13-infected mice. Averages ± SEM are shown (A). Data are pooled from three independent experimental repeats with n = 3–4 mice/group (A). (B–E) RNA sequencing was performed in a total of two independent experiments, in which each sequenced sample consists of IECs pooled from three mice. PCA (B) and DEGs (C–E) were calculated by DESeq2. (A) Kruskal–Wallis test with Dunn’s correction for multiple comparisons. (C) Pathway enrichment was determined by GSEA (P < 0.05; FDR < 0.25). *, P <0.05; **, P <0.01; ***, P <0.001; ****, P <0.0001. FC, fold change; p.adj, adjusted P value; PC, principal component.