Deleterious versus protective autoimmunity in multiple sclerosis
[Display omitted] •Deleterious autoimmunity in MS is mediated by auto-reactive Th1, Th9 and Th17 cells.•The dominant Th response in MS is dependent on patient’s individual characteristics.•Th cell induced microglia switch toward inflammatory phenotype is crucial in MS.•Autoimmunity mediated by Th2 a...
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Veröffentlicht in: | Cellular immunology 2015-08, Vol.296 (2), p.122-132 |
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Sprache: | eng |
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Zusammenfassung: | [Display omitted]
•Deleterious autoimmunity in MS is mediated by auto-reactive Th1, Th9 and Th17 cells.•The dominant Th response in MS is dependent on patient’s individual characteristics.•Th cell induced microglia switch toward inflammatory phenotype is crucial in MS.•Autoimmunity mediated by Th2 and T regulatory cells exhibits protective effects.•The failure to perform adequate protective autoimmunity is associated with MS.
Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disorder of central nervous system, in which myelin specific CD4+ T cells have a central role in orchestrating pathological events involved in disease pathogenesis. There is compelling evidence that Th1, Th9 and Th17 cells, separately or in cooperation, could mediate deleterious autoimmune response in MS. However, the phenotype differences between Th cell subpopulations initially employed in MS pathogenesis are mainly reflected in the different patterns of inflammation introduction, which results in the development of characteristic pathological features (blood–brain barrier disruption, demyelination and neurodegeneration), clinically presented with MS symptoms. Although, autoimmunity was traditionally seen as deleterious, some studies indicated that autoimmunity mediated by Th2 cells and T regulatory cells could be protective by nature. The concept of protective autoimmunity in MS pathogenesis is still poorly understood, but could be of great importance in better understanding of MS immunology and therefore, creating better therapeutic strategies. |
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ISSN: | 0008-8749 1090-2163 |
DOI: | 10.1016/j.cellimm.2015.04.006 |