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Updated: Oct 10, 2026

Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
The myelin oligodendrocyte glycoprotein (MOG): a model for antibody-mediated demyelination in experimental autoimmune
A Stefferl1, U Brehm, C Linington
1Max-Planck-Institute for Neurobiology, Planegg-Martinsried, Federal Republic of Germany.
Abstract:
The myelin oligodendrocyte glycoprotein (MOG) is a major target for autoantibody mediated demyelination in experimental autoimmune encephalomyelitis (EAE). In the current review we discuss the epitope specificity of this antibody response, in particular evidence suggesting that pathogenic anti-MOG antibodies are preferentially directed against conformation-dependent epitopes present on the extracellular immunoglobulin domain of the protein. Surprisingly, recent data suggest that this autoimmune response is in part regulated by polymorphisms in the MOG gene itself, an observation that may have important implications for the genetic and immunological stratification of patients with multiple sclerosis.
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