[Multiple sclerosis: review of main experimental data and pathogenic hypotheses].
The pathogenesis of multiple sclerosis (MS) is considered from three different viewpoints: genetic, viral and immunological. A genetic predisposition intervenes, as testified by the familial forms of MS and by the frequency of HLA A3B7 and DR2 groups in MS patients. The hypothesis of an inherited enzyme deficiency in oligodendrocytes is discussed. Many viruses are known to induce demyelination in animals, and the intrathecal production of antibodies to measles virus as well as the in vitro discovery of DNA transcripts of this virus in patients are suggestive of a viral factor. Experimental allergic encephalomyelitis (EAE) and chronic EAE have made it possible to study the immune and other mechanisms which might be involved in MS. While the myelin basic protein and the M2 antigen appear to be the first antigen targets, the demyelinating agents in this model are antibodies to galactocerebroside. The factors responsible for demyelination in MS have not yet been elucidated, but the antibodies present in the cerebrospinal fluid do not seem to be demyelinating in vitro. Descriptions of the cells which constitute the lesions and of the antigen markers they express suggest that endothelial cells and astrocytes (possibly presenting antigens to lymphocytes) might play a part in the genesis of the lesions. Experiments concerning the modulation and suppression of EAE allow new therapeutic approaches to be envisaged.
Fressinaud
C
C
Centre de Neurochimie du CNRS, Strasbourg.
Sarliève
L L
LL
Vincendon
G
G
D000818:Animals; D000917:Antibody Formation; D004195:Disease Models, Animal; D006801:Humans; D007111:Immunity, Cellular; D009103:Multiple Sclerosis / Q000209:etiology* / Q000235:genetics / Q000276:immunology
Sclérose en plaques: revue des principales données expérimentales et des hypothèses pathogéniques.