Myelin oligodendrocyte glycoprotein (MOG) is located on the external surface of myelin, a membranous component of the central nervous system (CNS) that forms the insulating lipid layer around neurons. The major MOG splicing variant (a1 transcript) encodes a transmembrane protein with an extracellular domain of an Ig variable (IgV) fold. MOG IgV domains from the same or different cells dimerize and contribute to the organization and maintenance of the myelin sheath in neurons. The encepalitogenic T cells recognize MOG and its immunodominant epitopes (epitopes 1-22, 35-55 and 92-106 located at the dimer interface) as foreign antigens and cause the destruction of myelin (demyelination) leading to the clinical condition known as multiple sclerosis (MS). Recognition of the antigen takes place in the context of the trimolecular complex formed by HLA, MOGpeptides and TCR.
Peptides & proteins
163913-87-9, AKOS030228368, KS-00000090
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 tolerance (1).
(1) Androutsou, M.-E., Tapeinou, A., Vlamis-Gardikas, A. & Tselios, T. Med. Chem. 14, 120–128 (2018)
2 582.0 Da
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. The immunodominant 35-55 epitope of MOG (MOG 35-55) is a primary target for both cellular and humoral immune responses (1). 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 CNS (1). Administration of MOG (35-55) peptide in mice produces anti-MOG antibodies that cause demyelination and a chronic Experimental Autoimmune Encephalomyelitis (1). 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 sclerosis (1). 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 tolerance (1).