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. 2024 Oct 11;300(11):107883. doi: 10.1016/j.jbc.2024.107883

Figure 3.

Figure 3

Role for Type I IFN signaling in transcriptomic changes in Irgm1-deficient macrophages. BMM from four distinct mice each for C57Bl/6 wild-type (WT), Irgm1−/− (Irgm1 KO), and IFNAR/Irgm1−/− (IFNAR/Irgm1 KO) were activated with IFN-γ for 24 h. mRNA was prepared and used for 16S RNA deep sequencing and Gene Set Enrichment Analysis. A, principal component analysis; B, the number of genes with statistically significant differences in expression in the indicated genotype relative to WT; LRT, FDR < 0.05. C, a heat map of select inflammatory chemokines and cytokines that have statistically significant increases in expression in Irgm1−/− BMM (relative to WT) that are reversed in IFNAR/Irgm1−/− BMM. The average fold change in expression is indicated. D, the number of gene pathways that were enriched in the indicated genotype relative to WT; fold change > 1.25; t test, P, FDR < 0.05. E, the number of ontologies that were enriched in the indicated genotype relative to WT; fold change > 1.25; t test, FDR < 0.05.