Abstract
Several different immunopathological mechanisms have been suggested to be involved in the destruction of myelin in inflammatory demyelinating diseases. They include destruction of oligodendrocytes by virus infection1 as well as immune mediated damage by macrophage products2, specific antibodies3 or T-lymphocytes4. To evaluate the validity of these concepts it is of critical importance to determine the fate of oligodendrocytes within the lesions5,6,7,8. This, however, was difficult and inconclusive because of the lack of specific and sensitive markers that allow the identification of oligodendrocytes in demyelinated plaques. Recently, new techniques became available to address this question, which have been applied in the present study.
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Keywords
- Multiple Sclerosis
- Experimental Allergic Encephalomyelitis
- Nick Translation
- Central Nervous System Tissue
- Inflammatory Demyelinating Disease
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Lassmann, H., Suchanek, G., Schmied, M. (1994). Mechanisms of DE — and Remyelination in Autoimmune Encephalomyelitis and Multiple Sclerosis. In: Salvati, S. (eds) A Multidisciplinary Approach to Myelin Diseases II. NATO ASI Series, vol 258. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2435-9_14
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DOI: https://doi.org/10.1007/978-1-4615-2435-9_14
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