The Mechanism of Suppression By a Protective Peptide in a Mouse Model of Multiple Sclerosis
نویسنده
چکیده
Multiple Sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS). MS is characterized by an immune response directed against myelin sheath. This immune response results in demyelination, which leads to the clinical symptoms of MS. It is accepted that MS is mediated by T helper 1/ T helper 17 immune responses. However, the role of B cells and antibodies (Abs) are still under debate. The primary animal model for MS is the experimental autoimmune encephalomyelitis (EAE) that is induced by immunizing animals with one of the myelin components. We previously showed that immunizing mice with the recombinant form of myelin oligodendrocyte glycoprotein (rMOG) results in ameliorated EAE compared to mice immunized with the encephalitogenic peptide MOG35-55. This amelioration was due to the presence of a cryptic epitope of MOG61-85 in rMOG as observed in previous peptide mapping analysis. We further investigated the mechanism of EAE amelioration in mice immunized with a longer
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