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Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
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Published on: June 21, 2018

TNF-alpha single nucleotide polymorphisms in atopic dermatitis.

Nasrin Behniafard1, Mohammad Gharagozlou, Elham Farhadi

  • 1Pediatrics Center of Excellence, Children's Medical Center.

European Cytokine Network
|January 19, 2013
PubMed
Summary
This summary is machine-generated.

Genetic variations in tumor necrosis factor-alpha (TNF-α) influence atopic dermatitis (AD) susceptibility. Specific TNF-α gene polymorphisms, particularly the GG genotype at positions -308 and -238, are strongly associated with increased risk in pediatric patients.

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Area of Science:

  • Immunogenetics
  • Dermatology
  • Molecular Biology

Background:

  • Atopic dermatitis (AD) is a complex inflammatory skin condition.
  • Tumor necrosis factor-alpha (TNF-α) is implicated in AD pathogenesis.
  • Cytokine gene single nucleotide polymorphisms (SNPs) may influence TNF-α levels and AD risk.

Purpose of the Study:

  • To investigate the association between TNF-α gene polymorphisms at positions -308 and -238 and susceptibility to atopic dermatitis in pediatric patients.
  • To determine the allelic, genotypic, and haplotypic associations of these TNF-α SNPs with AD.

Main Methods:

  • Case-control study involving 89 pediatric AD patients and 137 healthy controls.
  • Genotyping of TNF-α gene polymorphisms at positions -308 and -238 using polymerase chain reaction (PCR) with sequence-specific primers.
  • Statistical analysis to assess allelic, genotypic, and haplotypic associations.

Main Results:

  • The TNF-α -238/G allele (p<0.001) and TNF-α -308/G allele (p=0.003) showed significant positive allelic association with AD susceptibility.
  • The GG genotype at both TNF-α -238 and TNF-α -308 was significantly more prevalent in AD patients compared to controls (p<0.01).
  • The GG haplotype at TNF-α (-308,-238) was over-represented in AD patients (92.7%, p<0.001), while AG and GA haplotypes showed negative association (p<0.01).
  • The AG genotype of TNF-α -308, linked to high cytokine production, was decreased in AD patients, whereas the GG genotype, linked to low TNF-α production, was over-expressed.

Conclusions:

  • Specific TNF-α gene polymorphisms, particularly the GG genotype at -308 and -238, are significant genetic risk factors for atopic dermatitis in the studied pediatric population.
  • These findings highlight the role of TNF-α genetic variations in modulating AD susceptibility, potentially through altered cytokine production levels.
  • Further research into TNF-α pathway modulation could offer therapeutic targets for atopic dermatitis.