
Blood-retina barrier dysfunction in experimental autoimmune uveitis: the pathogenesis and therapeutic targets
- Jeongtae Kim Jiyoon Chun Meejung Ahn Kyungsook Jung Changjong Moon Tae-Kyun Shin
- 대한해부학회
- Anatomy and Cell Biology
- Vol.55(1)
- 등재여부 : KCI등재
- 2022.03
- 20 - 27 (8 pages)
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.
Introduction
Uveitogenic Antigens in Lewis Rats
Autoimmune T cells and Clonal Expansion of V Beta Genes
Homing of T Cells to the Uvea and Retina is a Pivotal Factor in EAU Pathogenesis
The RPE: A Barrier between Vessels and the Neural Retina
Therapeutic Strategies for EAU
Conclusion and Future Perspectives
ORCID
Author Contributions
Conflicts of Interest
Acknowledgements
References