Volume 15, Number 3 (6-2016)                   JRUMS 2016, 15(3): 257-280 | Back to browse issues page


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Etesam Z, Nemati M, Jafarzadeh A. The Role of T Lymphocyte Subsets in The Pathogenesis of Multiple Sclerosis. JRUMS. 2016; 15 (3) :257-280
URL: http://journal.rums.ac.ir/article-1-3185-en.html

Ph.D Rafsanjan University of Medical Sciences
Abstract:   (1473 Views)

Background and Objectives: Multiple sclerosis (MS) is an autoimmune neurodegenerative disease of the central nervous system (CNS). Although, the contribution of various cells such as  B cells, CD8+ T cells, microglia/macrophages, dendritic cells, asterocytes and mast cells in the pathogenesis of MS have been demonstrated, however, it seems that autoreactive myelin specific CD4+ T cells play a central role in pathological events contributing in MS pathogenesis. The aim was to evaluate the recent findings regarding the properties of T lymphocyte subsets and their roles in pathogenesis of MS disease. Functionally, distinct effector T cells are induced from naïve T cells upon antigenic stimulation, including Th1, Th2, Th17, Th22, Th9, and regulatory T (Treg) cells which are characterized based on their cytokine patterns. Of the activated T cells, Th1 cells secreting IFN-γ, Th17 cells producing IL-17, Th9 releasing IL-9, and Th22 secreting IL-22 play major roles in MS development, while Th2 cells producing IL-4, and Treg cells secreting IL-10 and TGF-β have been associated with a reduction of CNS inflammation and improvement of MS. The modulation of Th1, Th17, Th9 and Th22 cells activity and the promotion of Th2 and Treg cell-related responses can be more consider for immunological treatment of MS disease.

Key words: Multiple sclerosis, Th1, Th2, Th9, Th17, Th22, Treg

How to cite this article: Etesam Z, Nemati M, Jafarzadeh A. The Role of T Lymphocyte Subsets in The Pathogenesis of Multiple Sclerosis J Rafsanjan Univ Med Sci 2016; 15(3): 257-80. [Farsi]

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Type of Study: Review Article | Subject: ايمونولوژي
Received: 2016/02/21 | Accepted: 2016/05/24 | Published: 2016/07/10

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