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免疫与青光眼
引用本文:李维义,黄萍[综述],张绍敏,张纯[审校]. 免疫与青光眼[J]. 眼科研究, 2014, 0(5): 466-470
作者姓名:李维义  黄萍[综述]  张绍敏  张纯[审校]
作者单位:[1]北京大学第三医院眼科 视觉损伤与修复教育部重点实验室, 100191 [2]宾夕法尼亚州立大学医学院,美国17033
基金项目:国家自然科学基金项目(30772376、30371504、81300756、81041008、81170888)
摘    要:青光眼是不可逆盲的主要原因之一,是视神经的慢性退行性病变.视网膜神经节细胞(RGCs)凋亡和视神经纤维进行性丢失可导致青光眼患者视神经结构和视功能的损害.越来越多的临床和实验研究表明,免疫系统参与青光眼的神经变性过程.青光眼患者视神经变性中涉及免疫机制及免疫系统相关细胞的相互作用,包括眼免疫赦免环境的破坏、胶质细胞的异常激活、T细胞免疫的异常、Th1/Th2免疫失衡、自身抗原的产生、补体通路的激活、氧化应激反应、衰老等免疫因素及氧化应激放大的初始压力损伤,这些因素均可使青光眼视神经进一步损害.就眼的保护性免疫和免疫异常与青光眼的研究进展进行综述.

关 键 词:免疫性疾病  免疫  青光眼  免疫  视网膜神经节细胞  免疫  视神经疾病  免疫  自身抗原  免疫

Immunization and glaucoma
Affiliation:Li Weiyi, Huang Ping, Samuel Shaomin Zhang, Zhang Chun.( Key Laboratory of Vision Loss and Restoration of Ministry of Education, Department of Ophthalmology, Peking University Third Hospital, Peking University, Beijing 100191, China ; Penn State University College of Medicine, Hershey, PA , 17033, USA)
Abstract:Glaucoma,the major cause of global irreversible blindness,is a chronic neurodegenerative disease of the optic nerve.Apoptosis of retinal ganglion cells (RGCs) and progressive loss of optic nerve axons results in structural and functional deficits in glaucoma patients.Growing evidence obtained from clinical and experimental studies over the last decade strongly suggests the involvement of the immune system in the neurodegenerative process of glaucoma.This review aims to provide a perspective on the complex interplay of cellular events during glaucomatous neurodegeneration that involves aberrances or dysfunctions of immune system,such as ocular immune privilege,glial activation response,T cell-mediated immune responses,autoantibody-mediated immune responses,complement fixation reaction and aging,oxidative stress.The complex interplay of cellular events amplify the primary injury process and contribute to disease progression by oxidative stress and immune response,ultimately lead to cell death with loss of RGCs.
Keywords:Autoimmune disease/immunology  Glaucoma/immunology  Retinal ganglion cell/immunology  Optic nerve disease/immunology  Autoantigen/immunology
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