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Critical Reviews™ in Immunology

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ISSN Печать: 1040-8401

ISSN Онлайн: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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Immune-Mediated Oligodendrocyte Injury in Multiple Sclerosis: Molecular Mechanisms and Therapeutic Interventions

Том 22, Выпуск 5-6, 2002, 34 pages
DOI: 10.1615/CritRevImmunol.v22.i5-6.30
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Краткое описание

In this review, new insights into the immunopathogenesis of multiple sclerosis (MS) are discussed, with special focus on the potential mechanisms leading to neuroinflammation in MS—that is, the role of autoreactive T cells, infections, and neurodegenerative events. Oligodendrocytes are considered to be the target of autoimmune inflammation in the CNS of MS patients. Some important features of oligodendrocyte biology are discussed, together with the molecular mechanisms that are potentially involved in oligodendrocyte injury. These include injury mechanisms that might be executed by the adaptive and innate immune system, via cytokines and/or oligodendrocyte receptors, or as a consequence of nitrative and oxidative stress, and excitotoxicity. The mode of cell death of oligodendrocytes in MS is discussed, in addition to the mechanisms of axonal injury as observed in pathology- and imaging-based studies. Finally, recent progress in therapeutic strategies that may interfere with these pathological processes are reviewed, with a focus on repair strategies, such as gene therapy, antibody-mediated remyelination, and stem cell therapy.

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