Figure 1.
Panel A shows principal component analysis (PCA) of bulk RNA-sequencing of small intestinal ILC2s from Il33 KO, Il1rl1 KO, Il17rb KO, Crlf2 KO, and WT mice. PC1 (32 percent variance) and PC2 (23 percent variance) show clear separation between W T and alarmin signaling–deficient groups. This indicates that loss of each receptor changes the overall gene expression profile of ILC2s. Panel B shows gene ontology (GO) and KEGG pathway analysis of differentially expressed genes in the knockout mice. Enriched biological processes include “regulation of leukocyte differentiation”, “response to lipopolysaccharide”, “regulation of lymphocyte activation”, “cell–cell adhesion”, “cytokine production”, and “tissue remodeling”. KEGG pathways: “IL–17 signaling pathway”, “JAK-STAT signaling pathway”, “Th17 cell differentiation”, “Notch signaling pathway”, and “FoxO signaling pathway” are highlighted; dot size represents gene count. Panel C shows a heatmap of the top differentially expressed genes across samples from Il33 KO, Il1rl1 KO, Il17rb KO, Crlf2 KO, and WT mice. Rows represent genes and columns represent individual samples grouped by genotype. The z-score color scale (-4 to +4) ranges from blue (low expression) to red (high expression), showing distinct genotype-specific gene expression patterns.
Transcriptional profiling of ILC2s from various strains of alarmin-deficient mice. (A) PCA of bulk RNA-seq of small intestinal ILC2s isolated from Il33 KO, Il1rl1 KO, Il17rb KO, Crlf2 KO, and WT mice. (B) GO and KEGG pathway analysis of differentially regulated genes in the KOs from B. (C) Heatmap of the top differentially regulated genes in the KOs. Genes specific to each KO are indicated with different colors. Genes of interest are marked in red. (A–C)n = 4 mice per group.