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Sci Immunol. 2016 Sep 02;1(3). doi: 10.1126/sciimmunol.aaf8864.

The orphan nuclear receptor ROR alpha and group 3 innate lymphoid cells drive fibrosis in a mouse model of Crohn's disease.

Science immunology

Bernard C Lo, Matthew J Gold, Michael R Hughes, Frann Antignano, Yanet Valdez, Colby Zaph, Kenneth W Harder, Kelly M McNagny

Affiliations

  1. The Biomedical Research Centre, University of British Columbia, V6T 1Z3.
  2. STEMCELL Technologies Incorporated, Vancouver, British Columbia, V6A 1B6.
  3. Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3800, Australia.
  4. Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, V6T 1Z3.

PMID: 28670633 PMCID: PMC5489332 DOI: 10.1126/sciimmunol.aaf8864

Abstract

Fibrosis is the result of dysregulated tissue regeneration and is characterized by excessive accumulation of matrix proteins that become detrimental to tissue function. In Crohn's disease, this manifests itself as recurrent gastrointestinal strictures for which there is no effective therapy beyond surgical intervention. Using a model of infection-induced chronic gut inflammation, we show that

Conflict of interest statement

Competing interests: The authors declare no competing financial interests.

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