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A. Takeuchi, Y. Usui, M. Takeuchi, T. Kezuka, M. Usui; The role of CCR5 chemokine receptor in the development of experimental autoimmune uveoretinitis in mice . Invest. Ophthalmol. Vis. Sci. 2004;45(13):548.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Th1–type T cells have been known to act as effector cells in human uveoretinitis with autoimmune etiology and in the experimental autoimmune uveoretinitis (EAU). CCR5, which is a chemokine receptor expressed on Th1 cells, is pivotal for their migration to the site of inflammation. In this study, we investigated whether deficiency of CCR5 suppresses EAU. Methods: Wild type or CCR5 KO B6 mice were immunized with 200 µg of human IRBP peptide 1–20 (hIRBP–p) emulsified in complete Freund's adjuvant in order to induce EAU. The eyes were enucleated 21 days after IRBP immunization to evaluate ocular inflammation histologically. In addition, cells of draining lymph nodes and the spleen cells were also collected and stimulated in vitro with hIRBP–p. T cell proliferation responses were analyzed by [3H]–thymidine uptake and production of IL–6, IL–10, IL–12, IFN–γ, TNFα, and MCP–1 measured by cytometric bead array under stimulation with hIRBP–p. Results: Surprisingly, massive cell infiltration into the eye was observed in CCR5 KO mice, and was histopathologically much more severe than that in wild type mice. Moreover, T cell proliferation responses and secretion of IL–6, TNFα, IFN–γ, and MCP–1 were enhanced, and IL–10 production was reduced in CCR5 KO mice compared with wild type mice. Conclusions: These results suggest that the recruitment of Th1–type T cells via CCR5 may contribute to amelioration of EAU in mice.
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