Interleukin 23 in Crohn's Disease


Creative Commons License

Eken A. , Singh A. K. , Oukka M.

INFLAMMATORY BOWEL DISEASES, cilt.20, ss.587-595, 2014 (SCI İndekslerine Giren Dergi) identifier identifier identifier

Özet

Crohn's disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract, and it has a growing incidence in Western societies. IL-23 receptor variants have been identified as susceptibility or resistance factors for CD in genome-wide association studies. Accordingly, IL-23 is required for the development of experimental inflammatory bowel disease in many murine models. IL-23 receptor is expressed by both innate and adaptive immune cells, which include Th17, natural killer T, gamma delta T cells, and ROR gamma t(+) innate lymphoid cells all of which are capable of secreting IL-17A, IL-17F, IL-22, and interferon-gamma upon IL-23 stimulation. During the past decade, pathogenic and protective roles have been described for these cytokines in the inflammatory bowel disease pathogenesis. More recently, innate lymphoid cells have been implicated in disease development. In this review, we have summarized and discussed these findings with an emphasis not only on the contribution of Th17 but also on innate lymphoid cells to disease etiology.

Crohn's disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract, and it has a growing incidence in Western societies. IL-23 receptor variants have been identified as susceptibility or resistance factors for CD in genome-wide association studies. Accordingly, IL-23 is required for the development of experimental inflammatory bowel disease in many murine models. IL-23 receptor is expressed by both innate and adaptive immune cells, which include Th17, natural killer T, γδ T cells, and RORγt innate lymphoid cells all of which are capable of secreting IL-17A, IL-17F, IL-22, and interferon-γ upon IL-23 stimulation. During the past decade, pathogenic and protective roles have been described for these cytokines in the inflammatory bowel disease pathogenesis. More recently, innate lymphoid cells have been implicated in disease development. In this review, we have summarized and discussed these findings with an emphasis not only on the contribution of Th17 but also on innate lymphoid cells to disease etiology.