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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




Journal article


Expert Rev Gastroenterol Hepatol

Publication Date





223 - 237


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