Extended Data Fig. 8: Flow cytometry analysis of IL-22 production by ILC subsets in naive and colitic mice.
From: The IL-22–oncostatin M axis promotes intestinal inflammation and tumorigenesis
(a) Gating strategy used to identify CD45⁺ cells for analysis in Fig. 5c. (b) Ki67 expression in total ILCs (Lineage⁻, TCRα⁻, TCRγ−, CD90⁺) from colitic mice. n = 12 per condition from two independent experiments. Mann-Whitney U test. (c) IL-22 frequency in ILCs and T cells from colitic wild-type mice (H.h. + αIL-10R, day 7), measured by flow cytometry following PMA/ionomycin, IL-23, and IL-1β stimulation. n = 12; two experiments. (d) Cytokine profiles of ILC subsets: ILC3s (RORγt⁺), ILC1s (T-bet⁺, Eomes⁻), ILC2s (GATA3⁺), and NK cells (T-bet⁺, Eomes⁺); all Lineage⁻, TCRα⁻, TCRγ⁻. Assessed post-stimulation as in (c). n = 12; two experiments. (e, f) H.h. + αIL-10R colitis with anti-IL-12p40 or isotype control treatment (day 0, analysis on day 7). (e) Il22 expression in colon tissue by qPCR. (f) Histopathology scores. Data pooled from two experiments, n = 8 mice/group. (g, h) H.h. + αIL-10R colitis with anti-IL-23p19 or isotype control treatment (day 0, analysis on day 7). (g) Il22 expression in colon tissue by qPCR. (h) Histopathology scores. Data from one experiment, n = 6 mice/group. (i, j) Colitis induced in Rag2⁻/⁻ and Rag2⁺/⁺ mice for two weeks. (i) Colon histopathology scores. (j) Osmr expression in IECs normalized to steady-state controls. n = 6–8 mice/group from two independent experiments. All graphs show mean ± SEM; P-values determined by Mann-Whitney U test.
