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Immunopathogenesis of Ankylosing Spondylitis: An Updated Review



Daryabor G1 ; Harsini S2, 3 ; Rezaei N2, 3, 4
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2. Research Center for Immunodeficiencies, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  4. 4. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Acta Medica Iranica Published:2018

Abstract

Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory arthritis of unknown etiology, which belongs to a group of conditions known as spondyloarthropathies that comprises psoriatic arthritis, reactive arthritis, and enteropathic arthritis. AS causes pathologic new-bone formation in the axial skeleton, and leads to chronic pain, axial fusion, deformity, disability and skeletal fracture. Several genetic and environmental factors are known to be associated with AS. Notwithstanding the fact that a multitude of genes, such as human leukocyte antigen B27 (HLA-B27), endoplasmic reticulum-associated aminopeptidase 1 (ERAP1), and interleukin-23 receptor (IL-23R) have been previously speculated to be associated with individuals’ susceptibility to AS, no consensus about their precise role in the etiopathogenesis of AS has been reached. In the present study, we summarize the current literature on the immunogenetics of AS and contemporize the research advancement that has been made over the past decade. © 2018 Tehran University of Medical Sciences. All rights reserved.
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