青光眼及其视神经损害的免疫学研究进展  

Advance of immunological pathogenesis of glaucoma and glaucomatous neuropathy

作　　者：尹则琳(综述)[1] 郑日忠(审校)[1] 

机构地区：[1]天津市眼科医院天津市眼科学与视觉科学重点实验室天津市眼科研究所天津医科大学眼科临床学院,300020

出　　处：《中华实验眼科杂志》2013年第3期298-302,共5页Chinese Journal Of Experimental Ophthalmology

摘　　要：青光眼是一组以视网膜神经节细胞（RGCs）进行性丧失、视神经萎缩和视野缺损为特征的致盲性眼病，病理性眼压增高和眼内血液循环障碍是其主要的危险因素，其他危险因素还包括谷氨酸毒性、一氧化氮（NO）增加和氧化应激等，近年来发现免疫学因素也参与青光眼的发病及其视神经损害，主要的免疫学异常表现有热休克蛋白等自身抗体表达、眼内液及外周血中肿瘤坏死因子（TNF）等一些炎性细胞因子的升高等。从体液免疫学、细胞免疫学和细胞因子表达等方面就青光眼及其视神经损害的免疫学进展进行综述。Glaucoma is one of the leading causes of blindness worldwide. Its characteristics are chronic neurodegenerative disease of the optic nerve,such as apoptosis of retinal ganglion cells,progressive loss of optic nerve axons and visual fields defects. The elevated intraocular pressure and vascular insufficiency are considered as the major risk factors, and the other factors include the glutamate excitotoxicity, nitric oxide increasing and oxidative stress. In recent years,the immune system changes were found to be participated in the pathogenesis of glaucoma and its damages of optic nerve. The main findings are the autoantibodies of heat shock protein, the elevation of tumor necrosis factor and other proinflammatory cytokines in periphery blood and aqueous humor. The immunological advance of autoantibody,cellular immunity and eytokines in the glaucoma and its neuronal damage were reviewed.

关 键 词：青光眼 视网膜神经节细胞 免疫学 自身抗体 细胞因子 

分 类 号：R775[医药卫生—眼科]