Neuropathology in multiple sclerosis: new concepts
Identifieur interne : 001969 ( Main/Exploration ); précédent : 001968; suivant : 001970Neuropathology in multiple sclerosis: new concepts
Auteurs : Hans Lassmann [Autriche]Source :
- Multiple Sclerosis [ 1352-4585 ] ; 1998-06.
English descriptors
- Teeft :
- Axon, Axonal, Axonal damage, Axonal loss, Cytokine, Demyelinated, Demyelinated plaques, Demyelinating, Demyelinating antibodies, Demyelinating lesions, Demyelination, Encephalitogenic, Encephalomyelitis, Experimental models, Glycoprotein, Immune, Immune reaction, Lassmann, Lesion, Macrophage, Metabolic instability, Multiple sclerosis, Multiple sclerosis lesions, Multiple sclerosis pathology, Multiple sclerosis plaques, Myelin, Myelin oligodendrocyte glycoprotein, Myelin sheaths, Nature genetics, Neurol, Neuropathology, Oligodendrocyte, Plaque, Proc natl acad, Remyelination, Sclerosis, Sclerosis lesions, Sclerosis patients, Selective destruction, Transgenic mice, Tumor necrosis factor, Virus infection.
Abstract
Multiple sclerosis lesions are characterized by inflammation, demyelination and a variable degree of axonal loss. The patterns of inflammation in MS lesions are compatible with a T-lymphocyte mediated immune reaction. The formation of demyelinated plaques, however, seem to require additional immunological mechanisms. In this review evidence is discussed for a pathogenetic role of demyelinating antibodies, toxic macrophage products, cytotoxic T-cells as well as metabolic disturbances of oligodendrocytes. It is suggested that the pathological heterogeneity regarding the patterns and extent of demyelination, remyelination and axonal loss may be the outcome of variable dominant immunopathogenetic mechanisms in different multiple sclerosis patients.
Url:
DOI: 10.1177/135245859800400301
Affiliations:
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Le document en format XML
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