Abstract
The identification of myelin oligodendrocyte glycoprotein (MOG) as a target for autoantibody-mediated demyelination in experimental autoimmune encephalomyelitis (EAE) resulted in the re-evaluation of the role of B cell responses to myelin autoantigens in the immunopathogenesis of multiple sclerosis. MOG is a central nervous system specific myelin glycoprotein that is expressed preferentially on the outermost surface of the myelin sheath. Although MOG is only a minor component of CNS myelin it is highly immunogenic, inducing severe EAE in both rodents and primates. In rat and marmoset models of MOG-induced EAE demyelination is antibody-dependent and reproduces the immunopathology seen in many cases of MS. In contrast, in mice inflammation in the CNS can result in demyelination in the absence of a MOG-specific B cell response, although if present this will enhance disease severity and demyelination. Clinical studies indicate that autoimmune responses to MOG are enhanced in many CNS diseases and implicate MOG-specific B cell responses in the immunopathogenesis of multiple sclerosis. This review provides a summary of our current understanding of MOG as a target autoantigen in EAE and MS, and addresses the crucial question as to how immune tolerance to MOG may be maintained in the healthy individual. (C) 2001 Wiley-Liss, Inc.
Original language | English |
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Pages (from-to) | 220-234 |
Number of pages | 14 |
Journal | Glia |
Volume | 36 |
DOIs | |
Publication status | Published - 2001 |
Keywords
- demyelination
- central nervous system
- autoantibodies
- immunological tolerance
- EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
- CENTRAL-NERVOUS-SYSTEM
- MOG-INDUCED EAE
- MAJOR HISTOCOMPATIBILITY COMPLEX
- ANTIBODY-MEDIATED DEMYELINATION
- MYELIN/OLIGODENDROCYTE GLYCOPROTEIN
- BASIC-PROTEIN
- IL-6-DEFICIENT MICE
- COMMON MARMOSETS
- LEWIS RAT