Tezel Gülgün, Wax Martin B
Kentucky Lions Eye Center, University of Louisville School of Medicine, Louisville, Ky., USA.
Chem Immunol Allergy. 2007;92:221-227. doi: 10.1159/000099273.
Glaucoma is a chronic neurodegenerative disease of the optic nerve, in which apoptosis of retinal ganglion cells (RGCs) and progressive loss of optic nerve axons result in structural and functional deficits in glaucoma patients. This neurodegenerative disease is indeed a leading cause of blindness in the world. The glaucomatous neurodegenerative environment has been associated with the activation of multiple pathogenic mechanisms for RGC death and axon degeneration. Growing evidence obtained from clinical and experimental studies over the last decade also strongly suggests the involvement of the immune system in this neurodegenerative process. Paradoxically, the roles of the immune system in glaucoma have been described as either neuroprotective or neurodestructive. A balance between beneficial immunity and harmful autoimmune neurodegeneration may ultimately determine the fate of RGCs in response to various stressors in glaucomatous eyes. Based on clinical data in humans, it has been proposed that one form of glaucoma may be an autoimmune neuropathy, in which an individual's immune response facilitates a somatic and/or axonal degeneration of RGCs by the very system which normally serves to protect it against tissue stress.
青光眼是一种视神经的慢性神经退行性疾病,其中视网膜神经节细胞(RGCs)的凋亡和视神经轴突的逐渐丧失导致青光眼患者出现结构和功能缺陷。这种神经退行性疾病确实是全球失明的主要原因。青光眼性神经退行性环境与导致RGC死亡和轴突退化的多种致病机制的激活有关。过去十年从临床和实验研究中获得的越来越多的证据也强烈表明免疫系统参与了这一神经退行性过程。矛盾的是,免疫系统在青光眼中的作用被描述为具有神经保护作用或神经破坏作用。有益免疫和有害自身免疫性神经退行性变之间的平衡最终可能决定RGCs在青光眼眼中应对各种应激源时的命运。基于人类临床数据,有人提出一种形式的青光眼可能是一种自身免疫性神经病变,其中个体的免疫反应通过通常用于保护其免受组织应激的系统促进RGCs的体细胞和/或轴突退化。