T- and B-cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis

A. Iglesias, J. Bauer, T. Litzenburger, A. Schubart, Christopher Linington

    Research output: Contribution to journalArticle

    221 Citations (Scopus)

    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 languageEnglish
    Pages (from-to)220-234
    Number of pages14
    JournalGlia
    Volume36
    DOIs
    Publication statusPublished - 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

    Cite this

    T- and B-cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis. / Iglesias, A.; Bauer, J.; Litzenburger, T.; Schubart, A.; Linington, Christopher.

    In: Glia, Vol. 36, 2001, p. 220-234.

    Research output: Contribution to journalArticle

    Iglesias, A. ; Bauer, J. ; Litzenburger, T. ; Schubart, A. ; Linington, Christopher. / T- and B-cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis. In: Glia. 2001 ; Vol. 36. pp. 220-234.
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    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.",
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    AU - Linington, Christopher

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    AB - 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.

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