Fig. 6: NCR+ ILC are expanded in CPI-colitis.

a Distribution of gene expression changes in ILC clusters (ILC2s and NCR+ ILC1/3 s) from mice with CPI-induced colitis (n = 3) vs those from control wild-type BALB/c mice (n = 3). Gene were ranked by decreasing log fold changes and shown as circled coloured according to the associated false discovery rate. b Violin plots showing the expression levels of cytokines across the two ILC clusters in wild-type BALB/c control mice (n = 3) and mice with CPI-induced colitis (n = 3). c Pathways, identified by scanning the Hallmark gene signature dataset using GSEA, significantly upregulated (FDR < 0.05) in the two ILC clusters in mice with CPI-induced colitis (n = 3) vs control mice (n = 3). d Upstream regulators predicted to mediate the gene expression changes in CPI-induced colitis vs control samples from both ILC clusters. e Representative flow cytometry plots and (f) summary dot plot showing IFNγ and IL-17A cytokine production from Lin- IL-7R+ ILCs in wild-type mice treated with CPI-colitis (n = 7) compared to untreated mice (n = 8). The cells were restimulated with PMA and ionomycin for 3 h prior to analysis. g Colon and (h) spleen mass in untreated Rag2−/− mice (n = 12) and Rag2−/−mice given FMT only (n = 11) or FMT + CPI (n = 12). * P = 0.0413 ** P = 0.0022 **** P < 0.0001 Kruskal-Wallis Test with Dunn’s multiple comparison. i Gr-1+ neutrophil infiltration between untreated Rag2−/− mice (n = 8) and Rag2−/− mice given FMT only (n = 6) or FMT + CPI (n = 12). * P = 0.0366 Kruskal-Wallis Test with Dunn’s multiple comparison. j Representative flow cytometry plots and (k) summary dot plot showing IFNγ and IL-17A cytokine production from Lin- IL-7R+ ILCs in Rag2−/− mice treated with CPI-colitis (n = 4) compared to untreated control mice (n = 4). The cells were restimulated with PMA and ionomycin for 3 h prior to analysis. * P = 0.0286 Multiple Mann Whitney U Test. All experimental n in Fig. 6 are biologically independent mouse samples.