中华实验眼科杂志
中華實驗眼科雜誌
중화실험안과잡지
CHINESE JOURNAL OF EXPERIMENTAL OPHTHALMOLOGY
2014年
5期
466-470
,共5页
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
免疫性疾病/免疫%青光眼/免疫%視網膜神經節細胞/免疫%視神經疾病/免疫%自身抗原/免疫
면역성질병/면역%청광안/면역%시망막신경절세포/면역%시신경질병/면역%자신항원/면역
Autoimmune disease/immunology%Glaucoma/immunology%Retinal ganglion cell/immunology%Optic nerve disease/immunology%Autoantigen/immunology
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.
青光眼是不可逆盲的主要原因之一,是視神經的慢性退行性病變.視網膜神經節細胞(RGCs)凋亡和視神經纖維進行性丟失可導緻青光眼患者視神經結構和視功能的損害.越來越多的臨床和實驗研究錶明,免疫繫統參與青光眼的神經變性過程.青光眼患者視神經變性中涉及免疫機製及免疫繫統相關細胞的相互作用,包括眼免疫赦免環境的破壞、膠質細胞的異常激活、T細胞免疫的異常、Th1/Th2免疫失衡、自身抗原的產生、補體通路的激活、氧化應激反應、衰老等免疫因素及氧化應激放大的初始壓力損傷,這些因素均可使青光眼視神經進一步損害.就眼的保護性免疫和免疫異常與青光眼的研究進展進行綜述.
청광안시불가역맹적주요원인지일,시시신경적만성퇴행성병변.시망막신경절세포(RGCs)조망화시신경섬유진행성주실가도치청광안환자시신경결구화시공능적손해.월래월다적림상화실험연구표명,면역계통삼여청광안적신경변성과정.청광안환자시신경변성중섭급면역궤제급면역계통상관세포적상호작용,포괄안면역사면배경적파배、효질세포적이상격활、T세포면역적이상、Th1/Th2면역실형、자신항원적산생、보체통로적격활、양화응격반응、쇠로등면역인소급양화응격방대적초시압력손상,저사인소균가사청광안시신경진일보손해.취안적보호성면역화면역이상여청광안적연구진전진행종술.
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.