Amelioration of Experimental Autoimmune Encephalomyelitis Using the Myelin Oligodendrocyte Glycoprotein35-85 Peptide
نویسندگان
چکیده
Multiple sclerosis (MS) is a chronic debilitating disease affecting the central nervous system (CNS) in humans. Experimental autoimmune encephalomyelitis (EAE) remains the primary animal model of MS. MS/EAE are considered to be autoimmune diseases mediated by CD4 T helper (TH) cells. The role of B cells and antibody is under debate. Previous studies established B cell dependent (induced with recombinant myelin oligodendrocyte glycoprotein, [rMOG]) and B cell independent (induced with the MOG35-55 peptide) animal models of EAE. The identification of a unique B cell epitope (MOG amino acids [aa] 46-85) preceding the identified protective epitope (MOG61-85) led to the hypothesis that these antibodies against MOGaa46-85 were important in epitope selection in the rMOG model of EAE. Co-immunization of WT and B cell deficient (B cell) mice with MOG35-55 and MOG61-85 resulted in abrogation (B cell -/mice) or
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