Fig. 6: Abrogated baseline JAK-STAT signaling outside of the in vivo tissue context.
From: JAK-STAT signaling maintains homeostasis in T cells and macrophages

a, Outline of the experimental approach: ex vivo culture for 20 h with basal medium and 10% FCS without supplements or with M-CSF (to support macrophage viability) or with IFN-β stimulation either in the last 1.5 h before sample collection or for the full 20 h, followed by transcriptome profiling. b, Differential expression upon ex vivo culture compared with homeostatic conditions in wild-type cells. Bar plots display the mean and standard error of log2FCs. c, Enrichment or depletion of JAK-STAT-related gene sets among the differentially expressed genes from b. d, Enrichment or depletion of differentially expressed genes between JAK-STAT mutants and wild type from in vivo homeostatic conditions among the differentially expressed genes from b. For example, enrichment (red) of STAT1 knockout genes for IFN-β stimulation indicates that our homeostatic STAT1 target genes are preferentially induced by IFN-β stimulation. e, Summary of inferred receptor–ligand interactions in the spleen as inferred from the Tabula Muris dataset. Interactions where CD8+ T cells and macrophages represent targets (that is, express the receptor) are highlighted by black arrows. f, Selected ligand–receptor interactions of CD8+ T cells (top) and macrophages (bottom) with other types of immune cells. NES, normalized enrichment scores. P values in c, d and f are based on two-sided random sampling, corrected for multiple comparisons.