Vogt-Koyanagi-Harada综合征自身免疫反应机制的研究进展  

Research progress of autoimmune reaction mechanism in Vogt-Koyanagi-Harada syndrome

作　　者：张芷冰 陈博[1] Zhang Zhibing;Chen Bo(Department of Ophthalmology,Tongji Hospital Affiliated to Tongji Medical College of HUST,Wuhan 430000,China)

机构地区：[1]华中科技大学同济医学院附属同济医院眼科,武汉430000

出　　处：《中华眼底病杂志》2024年第6期485-490,共6页Chinese Journal of Ocular Fundus Diseases

基　　金：国家自然科学基金(面上项目)(82070991)。

摘　　要：Vogt-Koyanagi-Harada综合征(VKH)的发病机制至今尚未完全明确,目前研究主要认为VKH其实是一种自身免疫性疾病,特别是与T细胞发挥功能过程中所包含的各种信号传导通路介导的免疫反应相关。细胞免疫中各个T细胞亚群的平衡失衡对VKH发病的影响是近年来的研究热点方向,目前辅助性T细胞17/调节性T细胞平衡是临床研究的重点,对相关细胞通路,尤其是蛋白酪氨酸激酶-信号传导及转录激活因子蛋白通路、核因子-κB通路。而B细胞在VKH发病机制中的探索,也已通过各种靶向药物的成功应用初见成效。未来进一步筛选并定位到在VKH发病过程中异常调节或表达的基因或蛋白,早日全面深入地进行探究,有助于更好地阐明VKH的发病机制,并据此提升临床治疗方案的疗效以及开发新的治疗靶点。The pathogenesis of Vogt-Koyanagi Harada disease(VKH)has not yet been fully defined.Current studies mainly suggest that VKH is actually an autoimmune disease,especially related to the immune response mediated by various signal transduction pathways involved in the function of T cells.In recent years,the influence of the balance imbalance of various T cell subsets in cellular immunity on the pathogenesis of VKH has been a hot research direction.Currently,T helper cell 17/T regulatory cells,balance is the focus of clinical research,meanwhile,new discoveries and potential clinical treatment schemes have been made for related cellular pathways,particularly the Janus kinase/signal transducers and activators of transcription pathway and NF-kappa B pathway.The exploration of B cells in the pathogenesis of VKH has also achieved initial results through the successful application of various targeted drugs.In the future,further screening and localization of genes or proteins that are abnormally regulated or expressed in VKH,for which early comprehensive and indepth exploration will be helpful,thus improve the efficacy of clinical treatment programs and develop new therapeutic targets.

关 键 词：VOGT-KOYANAGI-HARADA综合征 发病机制 自身免疫反应 T细胞 细胞信号传导通路 综述 

分 类 号：R593.2[医药卫生—内科学]