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

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

Jeongtae Kim  1 , Jiyoon Chun  2 , Meejung Ahn  3 , Kyungsook Jung  4 , Changjong Moon  5 , Taekyun Shin  2
Affiliations
Review

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

Jeongtae Kim et al. Anat Cell Biol. .

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.

Keywords: Autoimmunity; Blood-retina barrier; Experimental autoimmune uveitis; Interphotoreceptor retinoid-binding protein; Retinal soluble antigen.

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Conflict of interest statement

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1
A schematic drawing of experimental autoimmune uveitis (EAU) pathogenesis. Modified from Kim et al. Neural Regen Res 2022;17:1604-8 [25].
See this image and copyright information in PMC

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