title: The IL-23/IL-17 pathway in inflammatory bowel disease.
abstract: 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.
authors.affiliation: Translational Gastroenterology Unit, Nuffield Department of Clinical Medicine, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK. alessandra.geremia@path.ox.ac.uk
authors.forename: Alessandra
authors.initials: A
authors.lastname: Geremia
authors.forename: Derek P
authors.initials: DP
authors.lastname: Jewell
mesh_terms: D000818:Animals; D003093:Colitis, Ulcerative / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D003424:Crohn Disease / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D006801:Humans; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism*; D053759:Interleukin-23 / Q000378:metabolism*; D007422:Intestines / Q000276:immunology* / Q000382:microbiology; D015398:Signal Transduction; D058504:Th17 Cells / Q000276:immunology
chemical_list: D018836:Inflammation Mediators; D020381:Interleukin-17; D053759:Interleukin-23