Abraham Clara, Cho Judy
Department of Medicine, Digestive Diseases, Yale University, New Haven, Connecticut 06520, USA.
Inflamm Bowel Dis. 2009 Jul;15(7):1090-100. doi: 10.1002/ibd.20894.
The IL-23/Th17 pathway has recently been identified to play a critical role in a number of chronic inflammatory diseases including inflammatory bowel disease (IBD). The identification in IBD patients of associations in IL23R and regions that include other genes in the IL-23/Th17 pathway has highlighted the importance of proper IL-23/Th17 pathway regulation in intestinal immune homeostasis. IL-23 plays a role in CD4+ Th17 lineage cells, characterized by IL-17 secretion and the expression of the transcription factor retinoic acid-related orphan receptor (ROR)gamma tau, and in other immune and nonimmune cells. The balance between effector T cell subsets, such as Th17 cells, and CD4+ T regulatory subsets is finely regulated; dysregulation of this balance can lead to inflammation and autoimmunity. As such, the IL-23/Th17 pathway contributes to immune responses that play a role in defenses to microbial infection, as well as in the intestinal inflammation observed in both animal models of colitis and human IBD.
白细胞介素-23/辅助性T细胞17（IL-23/Th17）信号通路最近被发现，在包括炎症性肠病（IBD）在内的多种慢性炎症性疾病中发挥关键作用。在IBD患者中，白细胞介素-23受体（IL23R）以及IL-23/Th17信号通路中包含其他基因的区域存在关联，这凸显了IL-23/Th17信号通路的正常调节在肠道免疫稳态中的重要性。IL-23在以分泌白细胞介素-17和表达转录因子视黄酸相关孤儿受体（ROR）γt为特征的CD4+辅助性T细胞17谱系细胞以及其他免疫和非免疫细胞中发挥作用。效应性T细胞亚群（如Th17细胞）与CD4+调节性T细胞亚群之间的平衡受到精细调节；这种平衡失调会导致炎症和自身免疫。因此，IL-23/Th17信号通路有助于免疫反应，在抵御微生物感染以及在结肠炎动物模型和人类IBD中观察到的肠道炎症中发挥作用。
