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KCI등재 학술저널

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

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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

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