Authors
Charles Egwuagu, Cheng-Rong Yu, Ahjoku Amadi-Obi, Xuebin Liu, Rashid Mahdi, and Yun Sang Lee
Summary
Expression of IL-17 in mouse PBMC, lymph node and retina is temporally correlated with progression of experimental autoimmune uveoretinitis (EAU). Uveitis is a diverse group of intraocular inflammatory diseases that cause severe visual loss and morbidity and is characterized by inflammatory attack of the uvea as well as the neuroretina 1. The disease may be of infectious or putative autoimmune etiology. The latter include birdshot retinochoroidopathy, sympathetic ophthalmia, Behçet’s disease, Vogt-Koyanagi-Harada syndrome, and ocular sarcoidosis 1. Understanding the immunopathogenic mechanisms of uveitis has benefited enormously by the development of an animal model of uveitis, experimental autoimmune uveitis (EAU). EAU is a predominantly a T cell-mediated intraocular inflammatory disease induced in susceptible species by active immunization with ocular-specific proteins (or peptides derived from them) and is transferable to naive syngeneic animals by injection of in vitro-activated CD4+, MHC class II-restricted T cell lines specific to retinal Ags 2-4. The two major uveitogenic retinal proteins are S-Ag (also termed “arrestin”) and interphotoreceptor retinoid-binding protein (IRBP) 2-4. In this study, we have used the EAU mouse model to further establish that TH17 cells are involved in pathogenic mechanisms of uveitis by showing that EAU can be ameliorated by treatment with antibody to IL-17.Further details
The protocol was published on Protocol Exchange in 2007. To see the entire protocol, click on the source link.Advertisement
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