Abstract
The most extensively studied inflammatory demyelinating diseases are multiple sclerosis (MS) and the animal model, experimental autoimmune encephalomyelitis (RAE). Both are characterized by perivascular inflammation, edema, demyelination and reactive gliosis. In MS the formation of the lesion, which contains T-lymphocytes and macrophages, is generally acknowledged to be related to a cell-mediated immune (CMI) response, and it is known that EAE involves CMI mechanisms requiring T-cell sensitization to a central nervous system antigen. For the past dozen years we have used EAE to explore mechanisms by which such CMI reactions might initiate inflammation, edema and demyelination.
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© 1990 Springer-Verlag Berlin Heidelberg
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Norton, W.T., Brosnan, C.F., Cammer, W., Goldmuntz, E. (1990). Some Aspects of Mechanisms of Inflammatory Demyelination. In: Jeserich, G., Althaus, H.H., Waehneldt, T.V. (eds) Cellular and Molecular Biology of Myelination. NATO ASI Series, vol 43. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83968-9_7
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DOI: https://doi.org/10.1007/978-3-642-83968-9_7
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