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Titlebook: Advances in the Immunopathogenesis of Multiple Sclerosis; D. Gambi,P. A. Muraro,U. Ecari Conference proceedings 1999 Springer-Verlag Itali

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The contribution of magnetic resonance imaging to the understanding of multiple sclerosis pathogeneow pathological specificity of conventional, T2-weighted MRI inevitably limits its potential for defining the pathophysiology of MS [1], although enhancement on T1-weighted scans after the injection of gadolinium-DTPA (Gd) can be used as a reliable marker of blood-brain barrier (BBB) dysfunction [1]
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,The naïve and memory MBP-reactive CD4+ T cell repertoire: implications for the autoimmune concept irs of MBP [N-terminal (1–11, 1–19), central (87–106, 83–99, 87–99, 84–102), central (111–129, 115–125), C-terminal (143–168, 131–159)] are predominantly recognized in the context of MS-associated HLA-DR molecules [5–10].
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Processor-Controlled Fast Potentiostaty of MS lesions has suggested that different mechanisms may act in different patients, accounting for the variability observed in clinical course, immunological findings in peripheral blood and cerebrospinal fluid (CSF), and response to immunomodulatory treatments.
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Pierre M. Bersier,Jacques Bersiergents. After activation and upregulation of adhesion molecules, these cells can cross the blood-brain barrier; after reactivation by myelin antigens either directly or via the recruitment of other cells, the activated T cells damage the myelin sheath and oligodendrocytes.
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Marta Sabou,Dietmar Winkler,Stefan Bifflor the involvement of neurons in the regulation of MHC expression emerged from several studies using neuronal transection models. These models permit the analysis of cellular responses occurring locally, as well as those distant from the primary lesion, without interfering with the blood-brain barrier.
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