The IL-23/IL-17 pathway in inflammatory bowel disease

被引:6
作者
Geremia, Alessandra [1 ]
Jewell, Derek P. [1 ]
机构
[1] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Clin Med, Translat Gastroenterol Unit, Oxford OX3 9DU, England
基金
英国惠康基金;
关键词
Crohn's disease; genes; IBD; IL-17; IL-23; inflammation; Th17; ulcerative colitis; GROWTH-FACTOR-BETA; GENOME-WIDE ASSOCIATION; ACTIVE CROHNS-DISEASE; T-HELPER-CELLS; ROR-GAMMA-T; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CHRONIC INTESTINAL INFLAMMATION; COLLAGEN-INDUCED ARTHRITIS; INNATE LYMPHOID-CELLS; CUTTING EDGE;
D O I
10.1586/EGH.11.107
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:223 / 237
页数:15
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