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Genetics and Immunodysfunction Underlying Behcet’S Disease and Immunomodulant Treatment Approaches Publisher Pubmed



Salmaninejad A1, 2, 3 ; Gowhari A4 ; Hosseini S2 ; Aslani S3 ; Yousefi M2 ; Bahrami T5 ; Ebrahimi M6 ; Nesaei A7 ; Zal M8
Authors
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Authors Affiliations
  1. 1. Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  2. 2. Medical Genetics Research Center, Student Research Committee, Department of Medical Genetics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  3. 3. Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
  5. 5. Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran
  6. 6. Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran
  7. 7. Department of Basic Sciences, Gonabad University of Medical Sciences, Gonabad, Iran
  8. 8. Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Journal of Immunotoxicology Published:2017


Abstract

Behcet’s disease (BD) is a chronic autoimmune condition primarily prevalent in populations along the Mediterranean Sea. The exact etiology of BD has not been fully explained yet, but the disease occurrence is associated with a genetic factor, human leukocyte antigen (HLA)-B51 antigen. Among the various immunodysfunctions that are found in BD, patients are increased neutrophil motility and superoxide production, as well as elevated production of tumor necrosis factor (TNF)-α and decreased production of interleukin (IL)-10. Elevated levels of inflammatory cytokines like IL-1 and IL-17 in BD have been found associated with aberrant expression of microRNA. Gene polymorphisms in BD patients have been observed in molecules involved in responses to pathogens that can ultimately modulate the host antimicrobial response. Moreover, several single nucleotide polymorphisms (SNPs) have been reported in genes encoding chemokines and adhesion molecules; many of these changes manifest as increases in vascular inflammation and vascular damage. Lastly, genetic and epigenetic changes have been suggested as involved in the pathogenesis of BD. Modifications in DNA methylation have been found in BD patient monocytes and lymphocytes, leading to adverse function of these cells. This review presents a comprehensive compilation of the literature with regard to the immunodysfunction underlying BD, as well as of the genetics, newly described clinical specifications and novel treatment strategies using immunomodulants based on the current understanding of BD. © 2017 The Author(s).
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