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Tumor Necrosis Factor-Alpha Single Nucleotide Polymorphisms in Juvenile Systemic Lupus Erythematosus Publisher Pubmed



Tahghighi F1 ; Ziaee V1, 2 ; Moradinejad MH2 ; Rezaei A3 ; Harsini S3 ; Soltani S4 ; Sadr M4 ; Mahmoudi M5 ; Aghighi Y6 ; Rezaei N2, 3, 4
Authors
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Authors Affiliations
  1. 1. Pediatric Rheumatology Research Group, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Molecular Immunology Research Center, Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. School of Nutrition and Dietetics, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Pediatrics, Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran

Source: Human Immunology Published:2015


Abstract

Background: Juvenile systemic lupus erythematosus (JSLE) is a multi-system autoimmune disorder of unknown origin. Given the importance of the contribution of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), towards the pathogenesis of JSLE, this study was performed to assess TNFA gene polymorphisms in a case-control study. Methods: Fifty nine patients with JSLE were enrolled in this study as case group and compared with healthy control subjects. The frequency of alleles, genotypes, and haplotypes of TNFA single-nucleotide polymorphisms (SNPs) at positions -308 and -238 were evaluated, using polymerase chain reaction with sequence-specific primers method. Results: The G allele at position -238 in TNFA promoter region was significantly more frequent in patients with JSLE than in the healthy controls (P value. <. 0.001), while the frequency of A allele at the same position was significantly lower than controls. Furthermore, a significant positive association for G/G genotype at the same position was detected in patients' group compared with control subjects (P value. <. 0.001). The GA haplotype of TNFA (positions -308, -238) was significantly less frequent in case group than in controls (P value. <. 0.001), while GG was the most frequent haplotype for TNFA in the patient group, compared to controls (P value. <. 0.01). Conclusions: Pro-inflammatory cytokine gene polymorphisms may influence susceptibility to JSLE. Particular TNFA gene variants are associated with JSLE and could be used as a genetic marker for susceptibility to JSLE. © 2015 American Society for Histocompatibility and Immunogenetics.
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