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This is the peer reviewed version of the following article: Mari, E. R., Moore, J. N., Zhang, G., & Rostami, A. (2015). Mechanisms of immunological tolerance in central nervous system inflammatory demyelination. Clinical and Experimental Neuroimmunology, 6(3), 264-274, which has been published in final form at DOI: 10.1111/cen3.12196. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.


Multiple sclerosis is a complex autoimmune disease of the central nervous system that results in a disruption of the balance between pro-inflammatory and anti-inflammatory signals in the immune system. Given that central nervous system inflammation can be suppressed by various immunological tolerance mechanisms, immune tolerance has become a focus of research in the attempt to induce long-lasting immune suppression of pathogenic T cells. Mechanisms underlying this tolerance induction include induction of regulatory T cell populations, anergy and the induction of tolerogenic antigen-presenting cells. The intravenous administration of encephalitogenic peptides has been shown to suppress experimental autoimmune encephalomyelitis and induce tolerance by promoting the generation of regulatory T cells and inducing apoptosis of pathogenic T cells. Safe and effective methods of inducing long-lasting immune tolerance are essential for the treatment of multiple sclerosis. By exploring tolerogenic mechanisms, new strategies can be devised to strengthen the regulatory, anti-inflammatory cell populations thereby weakening the pathogenic, pro-inflammatory cell populations.

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