Immune responses against the myelin/oligodendrocyte glycoprotein in experimental autoimmune demyelination

Myelin/oligodendrocyte glycoprotein (MOG) is a surface-exposed antigen of myelin and an important target for autoimmune responses which mediate inflammatory demyelination in the central nervous system. Experimentally, MOG induces strong pathogenic T cell responses in many strains of laboratory anima...

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Bibliographic Details
Published in:Journal of clinical immunology 2001-05, Vol.21 (3), p.155-170
Main Authors: von Büdingen, H C, Tanuma, N, Villoslada, P, Ouallet, J C, Hauser, S L, Genain, C P
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Antigens, Surface
Autoantibodies - biosynthesis
Autoantigens
B-Lymphocytes - immunology
Demyelinating Autoimmune Diseases, CNS - etiology
Demyelinating Autoimmune Diseases, CNS - immunology
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental - etiology
Encephalomyelitis, Autoimmune, Experimental - immunology
Humans
Mice
Molecular Sequence Data
Multiple Sclerosis - etiology
Multiple Sclerosis - immunology
Myelin Proteins
Myelin-Associated Glycoprotein - genetics
Myelin-Associated Glycoprotein - immunology
Myelin-Oligodendrocyte Glycoprotein
Primates
Rats
Sequence Homology, Amino Acid
T-Lymphocytes - immunology
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Summary:Myelin/oligodendrocyte glycoprotein (MOG) is a surface-exposed antigen of myelin and an important target for autoimmune responses which mediate inflammatory demyelination in the central nervous system. Experimentally, MOG induces strong pathogenic T cell responses in many strains of laboratory animals. Immunological studies in humans also identify MOG as a surprisingly prevalent antigenic molecule among the myelin proteins. In addition, the encephalitogenic properties of MOG are linked to the induction of antibody responses which have been demonstrated to directly promote central nervous system demyelination, a hallmark neuropathological feature in disorders such as human multiple sclerosis. Factors responsible for autoimmunity to MOG likely include genetic influences as well as other mechanisms, which are the subject of intense investigation. This article reviews experimental data currently available on specificity and pathogenic roles of T cell and antibody responses against MOG, which have implications relevant to multiple sclerosis and related disorders.
ISSN:0271-9142
1573-2592