Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The etiology of inflammatory bowel disease is unknown but available evidence suggests that a deregulated immune response towards the commensal bacterial flora is responsible for intestinal inflammation in genetically predisposed individuals. IL-23 promotes expansion and maintenance of Th17 cells, which secrete the proinflammatory cytokine IL-17 and have been implicated in the pathogenesis of many chronic inflammatory disorders. Recent studies have shown that IL-23 also acts on cells of the innate immune system that can contribute to inflammatory cytokine production and tissue inflammation. A role for the IL-23/IL-17 pathway in the pathogenesis of chronic intestinal inflammation in inflammatory bowel disease has emerged from both animal and human studies. Here we aim to review the recent advances in this rapidly moving field.

Original publication

DOI

10.1586/egh.11.107

Type

Journal article

Journal

Expert Rev Gastroenterol Hepatol

Publication Date

04/2012

Volume

6

Pages

223 - 237

Keywords

Animals, Colitis, Ulcerative, Crohn Disease, Humans, Immunity, Innate, Inflammation Mediators, Interleukin-17, Interleukin-23, Intestines, Signal Transduction, Th17 Cells