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Pd-1/Pd-L and Autoimmunity: A Growing Relationship Publisher Pubmed



Zamani MR1, 2 ; Aslani S1 ; Salmaninejad A2, 3 ; Javan MR4 ; Rezaei N1, 2, 5
Authors
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Authors Affiliations
  1. 1. Department of Immunology and Biology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  3. 3. Student Research Committee, Medical Genetics Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  4. 4. Department of Immunology, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran
  5. 5. Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran

Source: Cellular Immunology Published:2016


Abstract

Programmed death 1 (PD-1) and its ligands, namely PD-L1 and PD-L2, are one of the key factors responsible for inhibitory T cell signaling, mediating the mechanisms of tolerance and providing immune homeostasis. Mounting evidence demonstrates that impaired PD-1:PD-L function plays an important role in a variety of autoimmune diseases such as Type 1 diabetes (T1D), encephalomyelitis, inflammatory bowel diseases (IBD), Rheumatoid Arthritis (RA), autoimmune hepatitis (AIH), Behcet's disease (BD), myasthenia gravis (MG), autoimmune uveitis (AU), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), myocarditis, and ankylosing spondylitis (AS). By investigating the candidate genes, genome-wide association studies, and identification of single nucleotide polymorphisms (SNPs) in PD-1 gene in humans, it has been shown that there is a higher risk in relevant genetic associations with developing autoimmune diseases in certain ethnic groups. In this review we have tried to present a comprehensive role of PD-1:PD-L in all recently studied autoimmune diseases. © 2016 Elsevier Inc.
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