Induction of autoimmune encephalomyelitis and uveitis in B6 and (B6×SJL) mice by peptides derived from myelin/oligodendrocyte glycoprotein

Abstract

Previous studies have shown that immunization of the Lewis rat with myelin basic protein (MBP), an encephalitogenic antigen derived from the myelin sheath of the CNS, induced both experimental autoimmune encephalomyelitis (EAE) and anterior uveitis (AU). In the current study, we show that a major peptide derived from another encephalitogenic myelin protein—the myelin/oligodendrocyte glycoprotein (MOG35–55)—induced both encephalomyelitis and uveitis in (B6×SJL) F1 and wt-B6 mice. Pathological studies documented that an anterior uveitis was induced by MOG35–55. A similar disease pattern was induced by either active immunization with peptideMOG35–55 (pMOG35–55) or adoptive transfer of MOG35–55-specific T cells. The induced uveitis persisted for >60 days without remission. Our studies demonstrate for the first time that MOG is uveitogenic in mice that express the H-2 b genetic background. This new experimental model should provide a useful tool for the study of the pathogenesis of chronic AU and determination of the pathogenic mechanisms by which a large portion of MS patients develops uveitis.