The development of colitis in Il10^-/- mice is dependent on IL-22.

ABSTRACT: Mice deficient in the IL-10 pathway are the most widely used models of intestinal immunopathology. IL-17A is strongly implicated in gut disease in mice and humans, but conflicting evidence has drawn IL-17's role in the gut into question. IL-22 regulates antimicrobial and repair activities of intestinal epithelial cells (IECs) and is closely associated with IL-17A responses but it's role in chronic disease is uncertain. We report that IL-22, like IL-17A, is aberrantly expressed in colitic Il10^-/- mice. While IL-22⁺ Th17 cells were elevated in the colon, IL-22-producing ILC3s were highly enriched in the small intestines of Il10^-/- mice. Remarkably, Il10^-/-Il22^-/- mice did not develop colitis despite retaining high levels of Th17 cells an

SUBMITTER: Gunasekera DC 

PROVIDER: S-EPMC7566780 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature