白细胞介素-23及其受体与炎症性肠病

Interleukin-23,its Receptor and Inflammatory Bowel Disease

炎症性肠病(IBD)与遗传和免疫的关系一直是研究的热点。目前研究显示白细胞介素(IL)-23受体(IL-23R)基因多态性与克罗恩病(CD)的发病有关。IL-23是一个由IL-23p19和IL-12p40组成的异二聚体分子,属IL-12炎症因子家族成员。IL-23R的致病作用可能与通过IL-23-信号转导和转录激活因子(STAT)3-辅助性T细胞(Th)17-IL-17途径介导肠道免疫异常有关。在IBD的生物治疗方面,以IL-23配体或受体为靶点的单克隆抗体已取得初步成效。对IL-23/IL-23R基因及其致病途径的深入研究,将为寻找更多IBD生物治疗的靶点提供有力依据。

Genetic variant and immune disorder have been the hot spot in the studies of inflammatory bowel disease （IBD）. Recently, polymorphism of interleukin （IL）-23 receptor （IL-23R） has been demonstrated to play a key role in the pathogenesis of Crohn＇s disease （CD）. IL-23 is a member of IL-12 family, a heterodimer composed of IL-23p19 and IL- 12p40. The pathogenic mechanism of IL-23R to inflammation is possibly mediated by the disordered intestinal immune response through IL-23-signal transducer and activatom of transcription （STAT） 3-helper T cell （Th） 17-IL-17 pathway. Monoclonal antibodies targeting to the ligands or receptors of IL-23 have been shown to be prospective in the biotherapy of IBD. Further study on the IL-23IL-23R genes and their functions in the pathogenesis of IBD will help us find more treatment targets.