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The development of colitis in Il10−/− mice is dependent on IL-22
dc.contributor.author | Gunasekera, Dilini C | |
dc.contributor.author | Ma, Jinxia | |
dc.contributor.author | Vacharathit, Vimvara | |
dc.contributor.author | Shah, Palak | |
dc.contributor.author | Ramakrishnan, Amritha | |
dc.contributor.author | Uprety, Priyanka | |
dc.contributor.author | Shen, Zeli | |
dc.contributor.author | Sheh, Alexander | |
dc.contributor.author | Brayton, Cory F | |
dc.contributor.author | Whary, Mark T | |
dc.contributor.author | Fox, James G | |
dc.contributor.author | Bream, Jay H | |
dc.date.accessioned | 2021-10-27T20:28:50Z | |
dc.date.available | 2021-10-27T20:28:50Z | |
dc.date.issued | 2020 | |
dc.identifier.uri | https://hdl.handle.net/1721.1/135695 | |
dc.description.abstract | © 2020, Society for Mucosal Immunology. 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 and remaining colonized with colitogenic Helicobacter spp. Accordant with IL-22-induced IEC proliferation, the epithelia hyperplasia observed in Il10−/− animals was reversed in Il10−/−Il22−/− mice. Also, the high levels of antimicrobial IL-22-target genes, including Reg3g, were normalized in Il10−/−Il22−/− mice. Consistent with a heightened antimicrobial environment, Il10−/− mice had reduced diversity of the fecal microbiome that was reestablished in Il10−/−Il22−/− animals. These data suggest that spontaneous colitis in Il10−/− mice is driven by IL-22 and implicates an underappreciated IL-10/IL-22 axis in regulating intestinal homeostasis. | en_US |
dc.language.iso | en | |
dc.publisher | Springer Science and Business Media LLC | en_US |
dc.relation.isversionof | 10.1038/S41385-019-0252-3 | en_US |
dc.rights | Creative Commons Attribution-Noncommercial-Share Alike | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | en_US |
dc.source | PMC | en_US |
dc.title | The development of colitis in Il10−/− mice is dependent on IL-22 | en_US |
dc.type | Article | en_US |
dc.relation.journal | Mucosal Immunology | en_US |
dc.eprint.version | Author's final manuscript | en_US |
dc.type.uri | http://purl.org/eprint/type/JournalArticle | en_US |
eprint.status | http://purl.org/eprint/status/PeerReviewed | en_US |
dc.date.updated | 2021-09-13T14:23:18Z | |
dspace.orderedauthors | Gunasekera, DC; Ma, J; Vacharathit, V; Shah, P; Ramakrishnan, A; Uprety, P; Shen, Z; Sheh, A; Brayton, CF; Whary, MT; Fox, JG; Bream, JH | en_US |
dspace.date.submission | 2021-09-13T14:23:20Z | |
mit.journal.volume | 13 | en_US |
mit.journal.issue | 3 | en_US |
mit.license | OPEN_ACCESS_POLICY | |
mit.metadata.status | Authority Work and Publication Information Needed | en_US |
mit.metadata.status | Authority Work and Publication Information Needed |