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T. Yoshimura, K.-H. Sonoda, Y. Miyazaki, Y. Iwakura, T. Ishibashi, A. Yoshimura, H. Yoshida; The Distinct Role of IFN- and IL-17 on Experimental Autoimmune Uveitis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2627.
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© ARVO (1962-2015); The Authors (2016-present)
In experimental autoimmune uveoretinitis (EAU), a model of human autoimmune uveitis, activated T cells and macrophages move into the retina and cause tissue damage. A novel CD4+ subset distinct from Th1 and Th2 cells, termed Th17, has recently been described. Th17 cells produce IL-17, which exerts strong proinflammatory activities and autoimmune reaction. Although EAU have been traditionally classified as Th1-mediated disease involving IFN-γ production, in this study we analyzed the possible involvement of Th17 in EAU.
Mice (either wild-type or IL-17-deficient) were immunized with interphotoreceptor retinoid-binding protein peptide 1-20 in CFA with M. tuberculosis H37RA plus pertussis toxin; the course of EAU in IL-17KO mice, and effects of subretinal transfer of antigen-specific Th17 cells on the course of EAU were examined. Severity of EAU was evaluated clinically and histopathologically. Cytokine/chemokine expression in the eye and lymph node cells were examined by ELISA and RT-PCR methods.
IL-17-deficient mice showed early recovery from EAU compared to WT mice. At later phases, IFN-γ production in the eyes of IL-17-deficient mice or in lymph node cells is the same as that in WT mice. Subretinal transfer of in vitro-differentiated IRBP-specific Th17 cells induced EAU.
In addition to the previously reported roles of Th1 cells, IL-17+ T cells may also contribute to the development of EAU, especially at chronic phases of inflammation. Both Th1 and Th17 responses may drive pathogenesis of experimental autoimmune uveitis, and thus IL-17 also may be a target for therapy.
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