| First Author | Takeuchi A | Year | 2005 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 46 |
| Issue | 10 | Pages | 3753-60 |
| PubMed ID | 16186359 | Mgi Jnum | J:136933 |
| Mgi Id | MGI:3797354 | Doi | 10.1167/iovs.04-1429 |
| Citation | Takeuchi A, et al. (2005) CCR5-deficient mice develop experimental autoimmune uveoretinitis in the context of a deviant effector response. Invest Ophthalmol Vis Sci 46(10):3753-60 |
| abstractText | PURPOSE: Experimental autoimmune uveoretinitis (EAU) is an organ-specific, Th1-cell-mediated disease that targets the neural retina. CCR5 is a chemokine receptor expressed on Th1 cells that promotes their migration. In CCR5-deficient mice, we examined the role of CCR5 in the development of EAU induced by immunization with interphotoreceptor retinoid-binding protein (IRBP) peptide. METHODS: Wild-type or CCR5-deficient B6 mice were immunized with human IRBP peptide 1-20 (hIRBP-p), and the severity of EAU was assessed clinically and histologically. Splenocytes and cells of regional lymph nodes near the eye were collected and their proliferation and production of IL-6, IL-10, IFN-gamma, and CCL2 (MCP-1) in response to hIRBP-p stimulation were measured. Moreover, the intraocular levels of these cytokines were analyzed. RESULTS: Immunization with hIRBP-p induced EAU in CCR5-deficient mice with a severity comparable to that in wild-type mice. Histologically, T-cell infiltration of the eye was reduced, but granulocyte infiltration was augmented in CCR5-deficient mice. Although splenic T cells from CCR5-deficient mice produced IFN-gamma but not IL-10 on stimulation by hIRBP-p, T cells from the regional lymph nodes failed to produce both cytokines. IL-6 production in the eye and IL-6 and CCL2 production by splenic T cells were predominantly augmented in CCR5-deficient mice. CONCLUSIONS: The development of EAU is not prevented in CCR5-deficient mice. Although T-cell infiltration into the eye is apparently reduced in CCR5-deficient mice, the defect is compensated for by granulocyte infiltration, supposedly mediated by augmented intraocular production of IL-6. |
