Oxidative photoreceptor cell damage in autoimmune uveitis.
Oxidative photoreceptor cell damage in autoimmune uveitis.
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DOI：
10.1007/s12348-010-0007-5
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发表时间：
2010-10-30
影响因子：
2.9
通讯作者：
Rao, Narsing A
中科院分区：
文献类型：
--
作者：
Nguyen, Angeline M;Rao, Narsing A
葡萄膜炎包括广泛的眼内炎性疾病，并且常常导致不可逆的视力丧失。实验性自身免疫性葡萄膜炎（EAU）是用于研究人类葡萄膜炎的动物模型。先天性和适应性免疫反应都是EAU视网膜损伤的重要介导因素。先天性免疫应答首先发生在toll样受体的激活，其上调炎性细胞因子，导致氧化应激;随后，适应性免疫应答导致炎性细胞因子上调和线粒体氧化应激。在早期EAu中，线粒体DNA在炎性细胞浸润之前受损，并改变了Au中线粒体蛋白水平和线粒体功能。我们最近的研究证实了TLR 4在炎症细胞因子的产生、氧化DNA损伤的启动和线粒体氧化应激的诱导中的重要性。与EAU一样，交感性眼炎也会导致感光细胞线粒体氧化损伤。预防线粒体氧化应激和感光细胞凋亡的药物可能有助于预防葡萄膜炎中的视网膜损伤并保护视力。
Uveitis comprises an extensive array of intraocular inflammatory diseases and often results in irreversible visual loss. Experimental autoimmune uveitis (EAU) is an animal model used to study human uveitis. Both innate and adaptive immune responses are known to mediate retinal damage in EAU. The innate immune response occurs first with activation of toll-like receptors which upregulate inflammatory cytokines, leading to oxidative stress; subsequently, the adaptive immune response results in inflammatory cytokine upregulation and mitochondrial oxidative stress. In early EAU, mitochondrial DNA is damaged before inflammatory cellular infiltration and alters mitochondrial protein levels and the functions of mitochondria in AU. Our recent study confirms the importance of TLR4 in the generation of inflammatory cytokines, initiation of oxidative DNA damage, and induction of mitochondrial oxidative stress. Like EAU, sympathetic ophthalmia also results in photoreceptor mitochondrial oxidative damage. Agents that prevent mitochondrial oxidative stress and photoreceptor apoptosis may help prevent retinal damage and preserve vision in uveitis.