Fig. 7. Npm1OE protects against DSS-induced colitis.

a–e, Npm1^UTR−/− and littermate control mice were fed with 2.5% DSS for 7 days and allowed to recover for 3 days. Body weight (a), DAI (b), representative colon images (c), colon length (d) and colon histopathology (e) are shown (n = 4 individual mice). Scale bars = 500 μm (left) and 100 μm (right). f,g, LPLs were isolated from Npm1^UTR−/− and control mice on day 5 of administration of 2.5% DSS (n = 5 individual mice). The proportion of ILC3s (live CD45⁺Lin⁻RORγt⁺ cells) within the CD45⁺ population (f) and of IL-22-producing ILC3s (live CD45⁺Lin⁻RORγt⁺IL-22⁺ cells) with the ILC3 population (g) was determined by flow cytometry. h,i, Number of ILC3s (h) and IL-22⁺ ILC3s (i) in LPLs of Npm1^UTR−/− and control mice after DSS administration are depicted (n = 5 individual mice). j,k, IL-22 production by isolated colonic ILC3s from Npm1^UTR−/− and control mice on day 5 of administration of 2.5% DSS (j) and MNK3 cells in response to Npm1OE (k) was determined by ELISA (n = 3 biological samples). l–n, Control, Npm1^UTR+/−, Npm1^+/− and Npm1^UTR+/−Npm1^+/− mice were administered 2.5% DSS for 7 days and allowed to recover for 3 days. Representative images of the mouse colons (l), colon length (m) and colon histopathology (n) are shown (n = 5 individual mice). Scale bars = 500 μm (top) and 100 μm (bottom). o, IL-22 production by isolated colonic ILC3s from the indicated groups of mice was determined by ELISA (n = 3 individual mice). Data in d, f–k, m and o are representative of two independent experiments, shown as the means ± s.e.m., and statistical significance was determined by two-tailed unpaired Student’s t test (*P < 0.05, **P < 0.01 and ***P < 0.001).

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