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

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

Affiliations
  • 1Department of Anatomy, Kosin University College of Medicine, Busan,
  • 2Department of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju,
  • 3Department of Animal Science, College of Life Science, Sangji University, Wonju,
  • 4Functional Biomaterials Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup,
  • 5Department of Veterinary Anatomy, College of Veterinary Medicine and BK21 Plus Project Team, Chonnam National University, Gwangju, Korea

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.

Keyword

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

Figure

  • Fig. 1 A schematic drawing of experimental autoimmune uveitis (EAU) pathogenesis. Modified from Kim et al. Neural Regen Res 2022;17:1604-8 [25].


Reference

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