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实验性自身免疫性葡萄膜炎中的血视网膜屏障功能障碍:发病机制与治疗靶点。

Blood-retina barrier dysfunction in experimental autoimmune uveitis: the pathogenesis and therapeutic targets.

作者信息

Kim Jeongtae, Chun Jiyoon, Ahn Meejung, Jung Kyungsook, Moon Changjong, Shin Taekyun

机构信息

Department of Anatomy, Kosin University College of Medicine, Busan, Korea.

Department of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, Korea.

出版信息

Anat Cell Biol. 2022 Mar 31;55(1):20-27. doi: 10.5115/acb.21.227.

Abstract

Experimental autoimmune uveitis (EAU), an animal model of human uveitis, is characterized by infiltration of autoimmune T cells in the uvea as well as in the retina of susceptible animals. EAU is induced by the immunization of uveitogenic antigens, including either retinal soluble-antigen or interphotoreceptor retinoid-binding proteins, in Lewis rats. The pathogenesis of EAU in rats involves the proliferation of autoimmune T cells in peripheral lymphoid tissues and breakdown of the blood-retinal barrier, primarily in the uvea and retina, finally inducing visual dysfunction. In this review, we describe recent EAU studies to facilitate the design of a therapeutic strategy through the interruption of uveitogenic factors during the course of EAU, which will be helpful for controlling human uveitis.

摘要

实验性自身免疫性葡萄膜炎(EAU)是人类葡萄膜炎的动物模型,其特征是易感动物的葡萄膜以及视网膜中有自身免疫性T细胞浸润。在Lewis大鼠中,通过免疫致葡萄膜炎抗原(包括视网膜可溶性抗原或光感受器间类视黄醇结合蛋白)可诱导EAU。大鼠EAU的发病机制涉及外周淋巴组织中自身免疫性T细胞的增殖以及血视网膜屏障的破坏,主要发生在葡萄膜和视网膜,最终导致视觉功能障碍。在本综述中,我们描述了近期关于EAU的研究,以促进通过在EAU病程中阻断致葡萄膜炎因子来设计治疗策略,这将有助于控制人类葡萄膜炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c3f/8968224/6dd88925247c/acb-55-1-20-f1.jpg

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