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The Molecular Mechanisms of Vitamin A Deficiency in Multiple Sclerosis

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Abstract

Vitamin A, considered to be an essential nutrient, has important actions in immunological responses and the central nervous system (CNS). Neuroimmunological functions of vitamin A are mediated through its active metabolite, retinoic acid (RA). In the CNS, RA contributes to regeneration and plasticity, while also playing a key role in enhancing tolerance and reducing inflammatory responses by regulating T cell, B cell and dendritic cell populations. However, evidence has indicated lower plasma levels of vitamin A in patients with multiple sclerosis (MS). Vitamin A deficiency leads to dysregulation of immune tolerance and pathogenic immune cell production in this disease. Vitamin A may ameliorate MS pathogenesis through numerous mechanisms including a reduction in inflammatory processes by re-establishing the balance between pathogenic (Th1, Th17, Th9) and immunoprotective cells (Th2, Tregs), modulating B cell and dendritic cell function as well as increasing tolerance of autoimmunity and regeneration in the CNS. Thus, the results from the current review suggest that vitamin A can be considered as a potential treatment in MS disease management.

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Reza Dorosty-Motlagh, A., Mohammadzadeh Honarvar, N., Sedighiyan, M. et al. The Molecular Mechanisms of Vitamin A Deficiency in Multiple Sclerosis. J Mol Neurosci 60, 82–90 (2016). https://doi.org/10.1007/s12031-016-0781-0

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