Sun Deming

Kentucky Lions Eye Center， University of Louisville

The determination of the involvement of， and interactions between， different pathogenic T cell subsets is an indispensable step in the characterization of the pathogenesis of autoimmune disease. Our previous studies have investigated the clonal composition of autoreactive T cells， the activation requirements of T cells systemically and in the autoimmune organ， the ability of autoreactive T cell subsets to penetrate into the autoimmune organ， and the interactions of autoreactive T cell clones with parenchymal cells in the autoimmune organ. Using this expertise， we are now characterizing the newly recognized IL-17+ uveitogenic T cells and identify key factors promoting the activation and expansion of this pathogenic T cell subset. Our studies have shown that activation of IFN-+ and IL-17+ autoreactive T cells represent alternative pathogenic pathways of autoimmune uveitis and that increased activation of  T cells leads to an augmented Th17 response and enhanced EAU. During the development of EAU， the numbers of  T cells greatly increase not only in the peripheral lymphoid organs， but also in the inflamed eyes. Depletion of T cells from mice on the day of active induction of EAU reduces disease severity and reduces the number of IL-17+ IRBP-specific T cells induced by uveitogenic antigen. We also show that interaction between  and T cell subsets Results in the production of a large amount of IL-17. The characterization of the interaction between pathogenic T cell subsets should improve our understanding of disease pathogenesis and help in the design of new therapeutic measures for the effective treatment of related human diseases.

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