Publications

Detailed Information

IL-33 regulates the IgA-microbiota axis to restrain IL-1α–dependent colitis and tumorigenesis : IL-33 regulates the IgA-microbiota axis to restrain IL-1 alpha-dependent colitis and tumorigenesis

DC Field Value Language
dc.contributor.authorMalik, Ankit-
dc.contributor.authorSharma, Deepika-
dc.contributor.authorZhu, Qifan-
dc.contributor.authorKarki, Rajendra-
dc.contributor.authorGuy, Clifford S.-
dc.contributor.authorVogel, Peter-
dc.contributor.authorKanneganti, Thirumala-Devi-
dc.date.accessioned2024-05-16T01:58:45Z-
dc.date.available2024-05-16T01:58:45Z-
dc.date.created2023-05-08-
dc.date.created2023-05-08-
dc.date.created2023-05-08-
dc.date.issued2016-12-
dc.identifier.citationJournal of Clinical Investigation, Vol.126 No.12, pp.4469-4481-
dc.identifier.issn0021-9738-
dc.identifier.urihttps://hdl.handle.net/10371/203045-
dc.description.abstractInflammatory bowel diseases (IBD) affect over 5 million individuals in the industrialized world, with an increasing incidence rate worldwide. IBD also predisposes affected individuals to development of colorectal cancer, which is a leading cause of cancer-related deaths in adults. Mutations in genes encoding molecules in the IL-33 signaling pathway are associated with colitis and colitis-associated cancer (CAC), but how IL-33 modulates gut homeostasis is unclear. Here, we have shown that Il33-deficient mice are highly susceptible to colitis and CAC. Mechanistically, we observed that IL-33 promoted IgA production from B cells, which is important for maintaining microbial homeostasis in the intestine. Il33-deficient mice developed a dysbiotic microbiota that was characterized by increased levels of mucolytic and colitogenic bacteria. In response to chemically induced colitis, this microbial landscape promoted the release of IL-1 alpha, which acted as a critical driver of colitis and CAC. Consequently, reconstitution of symbiotic microbiota or IL-1 alpha ablation markedly ameliorated colitis susceptibility in Il33-deficient animals. Our results demonstrate that IL-33 promotes IgA production to maintain gut microbial homoeostasis and restrain IL-1 alpha-dependent colitis and CAC. This study therefore highlights modulation of IL-33, IgA, IL-1 alpha, and the microbiota as a potential therapeutic approach in the treatment of IBD and CAC.-
dc.language영어-
dc.publisherAmerican Society for Clinical Investigation-
dc.titleIL-33 regulates the IgA-microbiota axis to restrain IL-1α–dependent colitis and tumorigenesis-
dc.title.alternativeIL-33 regulates the IgA-microbiota axis to restrain IL-1 alpha-dependent colitis and tumorigenesis-
dc.typeArticle-
dc.identifier.doi10.1172/JCI88625-
dc.citation.journaltitleJournal of Clinical Investigation-
dc.identifier.wosid000390131900011-
dc.identifier.scopusid2-s2.0-85002926045-
dc.citation.endpage4481-
dc.citation.number12-
dc.citation.startpage4469-
dc.citation.volume126-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorKarki, Rajendra-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusAKKERMANSIA-MUCINIPHILA-
dc.subject.keywordPlusINTESTINAL INFLAMMATION-
dc.subject.keywordPlusULCERATIVE-COLITIS-
dc.subject.keywordPlusCOLON INFLAMMATION-
dc.subject.keywordPlusADAPTIVE IMMUNITY-
dc.subject.keywordPlusIMMUNOGLOBULIN-A-
dc.subject.keywordPlusENDOGENOUS IL-33-
dc.subject.keywordPlusCROHNS-DISEASE-
dc.subject.keywordPlusOPEN-LABEL-
dc.subject.keywordPlusRECEPTOR-
Appears in Collections:
Files in This Item:
There are no files associated with this item.

Related Researcher

  • College of Natural Sciences
  • School of Biological Sciences
Research Area Cytokine Storm, Host Defense, Innate Immunity in Metabolic and Inflammatory Diseases

Altmetrics

Item View & Download Count

  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Share