Changes in transcriptional profiles of splenic monocytes from Prf1^−/− mice infected with LCMV and treated with JAK1, JAK2, or combined JAK1/2 inhibitor. (A) Unsupervised clustering using multidimensional scaling of transcriptional profiles of splenic CD11b⁺Ly6C⁺ monocytes from mice infected with LCMV and treated with vehicle, itacitinib (120 mg/kg bid), fedratinib (60 mg/kg bid), or ruxolitinib (90 mg/kg bid) with 3 mice per group. (B) Venn diagram depicting the numbers of DEGs in itacitinib, fedratinib, or ruxolitinib vs vehicle-treated groups (adjusted P value <.05, |Log₂FC| >1). (C) Heat map of the significant DEGs in vehicle, itacitinib, fedratinib, or ruxolitinib treatment groups with clusters labeled on the y-axis. To the right of each cluster the enriched hallmark pathways are shown. (D) Dot plot of significantly up- (red) and downregulated (blue) hallmark gene sets (MSigDB v7.5.1) in LCMV-infected mice treated with itacitinib, fedratinib, or ruxolitinib compared with vehicle control (adjusted P value <.05 and NES >1). Gene sets in proliferation (purple), metabolic (pink), housekeeping (black), DNA damage repair (cyan), and immune (brown) pathways are colored respectively. (E-G) GSEA enrichment plots of the top 2 pathways in CD11b⁺Ly6C⁺ monocytes for itacitinib (E), fedratinib (F), or ruxolitinib (G) vs vehicle-treated controls. FC, fold change.