MOG35-55-biotin – Multiple sclerosis peptides

Biotin-MOG (35-55) peptide is the biotinylated version of Mouse MOG (35-55) peptide which is used to induce the Experimental Autoimmune Encephalomyelitis (EAE) mouse model for T-cell-mediated inflammatory demyelinating autoimmune diseases of the CNS. MOG35-55 - MEVGWYRSPFSRVVHLYRNGK - CAS 163913-87-9：Myelin oligodendrocyte glycoprotein (MOG) is a type I integral membrane glycoprotein of the immunoglobulin superfamily (Ig) found exclusively in mammals. The 26-28 kDa protein is located on the external surface of the oligodendrocyte membrane,mostly on the peripheral lamellae of myelin sheaths of the Central nervous system (CNS)1. MOG35-55 for EAE induction：The immunodominant 35-55 epitope of MOG (MOG 35-55) is a primary target for both cellular and humoral immune responses1. Anti-MOG antibodies and the abnormal activation of encepalitogenic T cells upon recognition of MOG (35-55) peptide cause the destruction of myelin sheath during Multiple sclerosis (MS),a common inflammatory autoimmune disorder of the CNS1. Although MOG is a minor component of the CNS,the 35-55 epitope of MOG (MOG 35-55) is strongly immunogenic and therefore is widely used for in vivo biological evaluation and immunological studies of the Experimental Autoimmune Encephalomyelitis (EAE),a mouse animal model for T-cell-mediated inflammatory demyelinating autoimmune diseases of the CNS1. Administration of MOG35-55 peptide in mice produces anti-MOG antibodies that cause demyelination and a chronic Experimental Autoimmune Encephalomyelitis1. Anti-MOG antibodies are observed in cerebrospinal fluid (CFS) and the serum of MS pateints. There is a direct correlation between the severity of the MS symptomes and anti-MOG titers. The progression of Multiple sclerosis is rapid and relapses occur more frequently in presence of anti-MOG antibodies. Therefore,anti-MOG antibodies are an indicator for the prognosis and progression of Multiple sclerosis1. They can be detected by MOG (35-55) epitope-coated ELISA for quantification. MOG (35-55)-induced EAE models can help elucidating the immunopathological mechanism of Multiple sclerosis and promote the developement of novel therapeutics. One therapeutic approach consists on the administration of a mixture of peptides,representing immunodominant epitopes of different myelin proteins including MOG peptide at a proper dose to modulate the immune response and induce tolerance1.

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