Interphotoreceptor retinoid binding protein peptide-induced uveitis in B10.RIII mice: Characterization of disease parameters and immunomodulation

被引:25
作者
Hankey, DJR
Lightman, SL
Baker, D
机构
[1] UCL, Dept Neurochem, Inst Neurol, Neuroinflammat Grp, London WC1N 1PJ, England
[2] UCL, Dept Clin Ophthalmol, Inst Ophthalmol, London, England
关键词
autoimmune disease; experimental autoimmune uveoretinitis; immunopathology; immunomodulation; uveitis; monoclonal antibody; in vivo animal models;
D O I
10.1006/exer.2000.0957
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Experimental autoimmune uveoretinitis (EAU) can be induced in the B1O.RIII mice following immunization with bovine interphotoreceptor retinoid binding protein (IRBP) and human IRBP161-180 peptide. This study examines the value of the human IRBP161-180 peptide model in the B1O.RIII mice. as a suitable model of EAU in order to examine immunotherapies, Having established a reliable and consistent immunization protocol of 25 mug peptide and no PTX, the time course of histopathology was performed. which graded both cellular and structural scores individually. Disease was typically of an acute nature. characterized by rapid onset of a massive inflammatory response. resulting in extensive damage to the rod outer segments (ROS) and neuronal layers. Treatment with potent immuno suppressive agents. CD4-specific monoclonal antibodies resulted in the inhibition of disease and a reduction in disease incidence. Treatment with p55-tumor necrosis factor receptor-Ig (p55-TNFR-Ig) fusion protein reduced structural damage to the retina despite a high level of cellular infiltration in the eye, suggesting that target organ damage in an acute model of EAU can be modulated. (C) 2001 Academic Press.
引用
收藏
页码:341 / 350
页数:10
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