Abstract
Many distinct lines of evidence suggest that immunopathological mechanisms are involved in onset und course of multiple sclerosis (MS). As examples, abnormally distributed immunoglobulins in the cerebrospinal fluid, shifts in T lymphocyte subset equilibria, and abnormalities in natural killer functions are commonly cited (McFarlin & McFarland, 1982; Waksman, 1983; Weiner & Hauser, 1982). Perhaps the most impressing argument in favor of an immunopathogenesis is, however, the morphological appearance of the MS lesion within the CNS white matter. Focal round cell infiltrations mainly around postcapillary venules, activation of astrocytes, and destruction of myelin are the key features. A practically identical lesion pattern is inducible by immunizing experimental animals with autologous white matter (Lassmann, 1983). The similarity between the inducible experimental autoimmune diesease and MS are so far the most compelling evidence for autoimmune mechanisms in the pathogenesis of MS.
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© 1986 ECSC, EEC, EAEC, Brussels and Luxembourg
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Wekerle, H. (1986). Molecular and Cellular Basis of Autoimmune Encephalitogenesis. In: Hommes, O.R. (eds) Multiple Sclerosis Research in Europe. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-4143-4_26
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DOI: https://doi.org/10.1007/978-94-009-4143-4_26
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