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ARTICLE
TNF-alpha single nucleotide polymorphisms in atopic dermatitis
1 Pediatrics Center of Excellence, Children’s Medical Center
2 Molecular Immunology Research Center; and Department of Immunology, School of Medicine
3 Hematology Department, School of Allied Medical Science
4 Growth and Development Research Center
5 Rheumatology Research Center
6 Research Center for Immunodeficiencies, Children’s Medical Center
Tehran University of Medical Sciences, Tehran, Iran
European Cytokine Network 2012, 23(4), 163-165. https://doi.org/10.1684/ecn.2012.0323
Accepted 05 September 2012;
Abstract
Tumor necrosis factor-alpha (TNF-α) could be considered as potential biomarkers in atopic dermatitis (AD), while its level could be influenced by cytokine single gene polymorphisms (SNP). This study was performed in 89 pediatric patients with AD and 137 controls to assess polymorphisms of the TNF-α gene at positions -308 and -238, using the polymerase chain reaction and the sequence-specific primers method. The highest positive allelic association that made the patients susceptible to AD was seen for TNF-α -238/G (p<0.001) and TNF-α -308/G (p = 0.003). The GG genotypes at TNF-α -238 and TNF-α -308, were both significantly higher in the patients with AD, compared to the controls (p<0.01). The GG haplotype at TNF-α (-308,-238) was seen in 92.7% of the patients, which was significantly higher than the controls (p<0.001), while a negative haplotypic association with AD was seen for TNF-α (-308, -238) AG and GA (p<0.01). This study showed that the AG genotype of TNF-α -308, associated with a high production of cytokines, was significantly decreased in patients with AD, while the low-producing GG genotype, which could lead to low production of TNF-α, was over-expressed in the atopic patients.Keywords
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Copyright © 2012 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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