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IL-23/IL-17通路及调节网络在葡萄膜炎发生中的作用

Role of IL-23/IL-17 pathway and regulatory network in the pathogenesis of uveitis

摘要葡萄膜炎是一类发病机制尚不完全清楚的致盲率较高的眼病。近年来,研究发现白细胞介素(IL)-23/IL-17通路在葡萄膜炎发生中起着重要作用。IL-23/IL-17信号通路以辅助性T细胞17活化为主线,作用于靶细胞,造成炎性因子、趋化因子的大量产生及视网膜色素上皮屏障功能的破坏,进而引起葡萄膜炎的发生。IL-23/IL-17通路受庞大的网络调节,多个正向及负向调节因子通过调节该通路引起免疫失调,从而参与葡萄膜炎的发生。IL-23/IL-17通路及调节网络中基因的多态性与葡萄膜炎密切相关,为研究葡萄膜炎的遗传发病机制提供了重要的基础。此外,临床试验已证实靶向IL-23/IL-17通路生物制剂的疗效,为葡萄膜炎的治疗提供了新的研究方向。本文对IL-23/IL-17通路及其生理功能进行概述,对葡萄膜炎中IL-23/IL-17通路及其调节网络正向、负向调节因子和基因多态性进行总结分析,并对葡萄膜炎中IL-23/IL-17通路生物制剂研究进展进行综述,以期加深对葡萄膜炎发病机制的认识,从而指导临床治疗。

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abstractsUveitis is an inflammatory disease, a leading cause of blindness, the pathogenesis of which is not fully understood.In recent years, it has been found that interleukin (IL)-23/IL-17 pathway plays an important role in the occurrence of uveitis.The IL-23/IL-17 pathway mainly acts on target cells through activating the T helper 17 cells, resulting in the production of inflammatory factors and chemokines as well as the damage of retinal pigment epithelium, which can cause uveitis.The IL-23/IL-17 pathway is regulated by a giant network, and the regulation of it by its positive and negative factors can lead to immune disorders and participate in the occurrence of uveitis.The polymorphism of genes in IL-23/IL-17 pathway and regulatory network is closely related to uveitis, which provides an important basis for the genetic pathogenesis of uveitis.In addition, clinical trials have confirmed the efficacy of biological agents targeting IL-23/IL-17 pathway, which provides a new research direction for the treatment of uveitis.The IL-23/IL-17 pathway and its physiological function, the positive and negative factors and gene polymorphism of IL-23/IL-17 pathway and its regulatory network in uveitis were summarized, and the research progress of biological agents of IL-23/IL-17 pathway in uveitis were reviewed in this article in order to deepen the understanding of the pathogenesis of uveitis and guide clinical practice.

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中华实验眼科杂志

中华实验眼科杂志

2021年39卷11期

1010-1016页

ISTICPKUCSCDCA

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