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S. Fujimura, T. Kaburaki, M. Haino, Y. Fujino, J. Numaga, A. Yoshida, H. Kawashima, M. Araie; Chemokine Receptor–CXCR3 Deficient Mice Develop Experimental Autoimune Uveitis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):977.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Experimental autoimmune uveitis (EAU) is a T cell–mediated disease that targets the neural retina and serves as a model of human uveitis. CXCR3, which is a chemokine receptor expressed on Th1 cells, has a pivotal role for their migration to the sites of inflammation. In this study, we investigated whether EAU is inducible in CXCR3–deficient mice(CXCR3KO). Methods: EAU was induced by immunizing wild–type C57BL/6 mice (n=11)and CXCR3KO C57BL/6 mice (n=9) with specific immunodominant peptides of human interphotoreceptor retinoid binding protein (hIRBP–p) with complete Freund's adjuvant (CFA). Fundoscopic evaluation for longitudinal follow–up of EAU was performed and scored. At day 21, all mice were sacrificed. The eyes were harvested for histopathological grading. Statistical analyses were performed by an independent Student's t–test. Results:Clinically, EAU developed in both wild–type and CXCR3KO mice. Fundoscopy revealed that 82% of wild–type mice developed EAU with average clinical EAU–score of 1.1±0.7 (average ± standard error), as compared to EAU–score of 2.4±0.7 in 100% of CXCR3KO mice. CXCR3KO mice had significantly more severe diseases than wild–type mice(p<0.01). Histopathological analyses of the eye tissues in CXCR3KO and wild–type mice revealed retinal lesions, including vasculitis, inflammatory cellular infiltration and damage to the photoreceptor cell layer. In most cases, histopathological grades of disease in CXCR3KO mice were higher than those in wild–type mice. Conclusions: Deficiency of CXCR3 in vivo did not affect the development of EAU. Signals via CXCR3 may not be required for the induction of EAU, but they may rather play a role for suppressing the activity of Th1 cells.
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