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首页> 外文期刊>Journal of Ophthalmic Inflammation and Infection >Oxidative photoreceptor cell damage in autoimmune uveitis
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Oxidative photoreceptor cell damage in autoimmune uveitis

机译：自身免疫性葡萄膜炎中氧化性感光细胞损伤

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摘要

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.
机译：葡萄膜炎包括广泛的眼内炎性疾病，通常导致不可逆的视力丧失。实验性自身免疫性葡萄膜炎（EAU）是用于研究人葡萄膜炎的动物模型。已知先天性和适应性免疫反应均可介导EAU中的视网膜损伤。先天免疫反应首先通过上调炎症细胞因子的toll样受体激活而发生，从而导致氧化应激。随后，适应性免疫反应导致炎症性细胞因子上调和线粒体氧化应激。在早期的EAU中，线粒体DNA在炎性细胞浸润之前受到破坏，并改变了AU中的线粒体蛋白水平和线粒体功能。我们最近的研究证实了TLR4在炎症细胞因子的产生，氧化性DNA损伤的起始以及线粒体氧化应激的诱导中的重要性。与EAU一样，交感性眼病也会导致光感受器线粒体的氧化损伤。预防线粒体氧化应激和光感受器凋亡的药物可能有助于预防视网膜损伤并保持葡萄膜炎的视力。

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