Molecular Basis of Multiple Sclerosis: The Immune System by Jane E. Libbey, Robert S. Fujinami (auth.), Roland Martin,

By Jane E. Libbey, Robert S. Fujinami (auth.), Roland Martin, Andreas Lutterotti (eds.)

Despite significant efforts by way of the medical group through the years, our realizing of the pathogenesis or the mechanisms of harm of a number of sclerosis continues to be restricted. hence, the present concepts for remedy and administration of sufferers are constrained of their efficacy. The mechanisms of tissue safeguard and service are most likely even much less understood. One reason behind those barriers is the big complexity of the ailment and each part of its pathogenesis, the mechanisms of tissue damage, the diagnostic tactics and eventually the efficacy of remedies and their uncomfortable side effects. the purpose of this publication is to check the newest advances made during this hugely advanced field.

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The initial acute demyelinating lesions are associated with viral replication within glial cells of the white matter with extensive infection of astrocytes and restricted infection (viral transcription without translation) of oligodendrocytes, resulting in a dramatic impairment of myelin metabolism. Progression of the chronic demyelinating lesions may be due to both the inflammatory immune reaction, in which the antiviral immune response destroys oligodendrocytes by means of a bystander mechanism, and the persistence of the virus (noncytolytic) in white matter areas outside of the lesions [reviewed in (Vandevelde and Zurbriggen 2005)].

Mice primed with UPLP and then challenged with phosphate-buffered saline (PBS) in CFA or with PLP139–151 in CFA developed clinical and pathological signs of CNS disease. Mice primed with UPLP and then challenged with recombinant vaccinia virus encoding b-galactosidase developed pathological signs of CNS disease without any clinical signs of the disease. In contrast, mice primed with PLPall and challenged with PBS in CFA did not develop pathological or clinical signs of the disease, thus indicating that the initial priming event may require efficient MHC class I presentation of the mimicking antigen which occurs with the ubiquitinated construct (Theil et al.

EBV-infected B cells, which could include CNS-reactive B cells, would not only produce pathogenic autoantibodies, but could also localize to the CNS where they could act as antigen-presenting cells (APC). These EBV-infected APC could present CNS antigens to CD4+ T cells, which have been activated by common systemic infections in the periphery, and which may be cross-reactive for CNS antigens, and which may be reactivated by the APC as they traffic through the CNS, thus promoting the survival of CNSreactive T cells within the CNS.

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