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The Role of Immune Regulatory Molecules in Multiple Sclerosis Publisher Pubmed



Afshar B1 ; Khalifehzadehesfahani Z1 ; Seyfizadeh N2 ; Rezaei Danbaran G3 ; Hemmatzadeh M4, 5 ; Mohammadi H6, 7
Authors
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Authors Affiliations
  1. 1. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Medical Oncology, National Center for Tumor Diseases, Heidelberg University Hospital, Heidelberg, Germany
  3. 3. Department of genetic, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
  4. 4. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran
  5. 5. Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  6. 6. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran
  7. 7. Department of Immunology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran

Source: Journal of Neuroimmunology Published:2019


Abstract

Multiple sclerosis (MS) is the most common demyelinating disease which mainly impacts the integrity of central nervous system (CNS). MS etiology is not clearly known but genetic, environmental factors and immune system are the most frequently explored risk factors. Adaptive immune responses have a critical role in MS pathogenesis in which auto-reactive T-cells and autoantibodies are main orchestrators. Immune responses are modulated by inhibitory molecules which regulates adaptive system activation and hemostasis interface. These molecules suppress immune responses through inhibition of cytokine secretion and T cell proliferation and subsequently reducing the inflammation and respective damage. Therefore the critical role of inhibitory molecules in regulating the healthy and safe immune responses make them very attractive target for immunotherapy. In this review paper, the role of inhibitory molecules expressed on the various immune cell types in MS pathogenesis and experimental autoimmune encephalomyelitis (EAE) animal model will be summarized. © 2019 Elsevier B.V.
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