期刊
CURRENT OPINION IN NEUROLOGY
卷 32, 期 3, 页码 313-319出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WCO.0000000000000685
关键词
demyelination; inflammation; multiple sclerosis; myelin oligodendrocyte glycoprotein; neurodegeneration
资金
- Medical University of Vienna, Austria
Purpose of review Research on multiple sclerosis (MS) pathogenesis and therapy is to a large extent driven by results obtained in experimental autoimmune encephalomyelitis (EAE). This approach provided deep insights into the mechanism of brain inflammation and immune mediated tissue injury and, thus, most of our currently established therapies for MS patients have been developed with profound contributions of experimental autoimmune research. Recent data, which are summarized in this review article, however, show important differences between EAE and MS. Recent findings EAE models perfectly reproduce a disease, now called myelin oligodendrocyte glycoprotein (MOG) antibody-associated inflammatory demyelinating disease, which, however, is different from classical MS. In MS, the inflammatory reaction in the brain is dominated by CD8(+) T-lymphocyte and CD20(+) B cells. Demyelination in MS appears to be triggered by soluble factors, produced by T cells and/or B cells, which are different from anti-MOG antibodies seen in EAE, and induce widespread MS like primary demyelination and tissue damage associated with oxidative injury, mitochondrial damage and subsequent 'virtual' hypoxia. Summary To define the antigenic target of the inflammatory reaction, the nature of the inflammatory response and the mechanisms of tissue injury are key topics of ongoing MS research.
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