Cytokine gene polymorphisms in allergic contact dermatitis

Contact Dermatitis. 2003 Feb;48(2):93-8. doi: 10.1034/j.1600-0536.2003.480208.x.

Abstract

Susceptibility to contact allergy may be influenced by genetically determined alterations in the production of pro- and anti-inflammatory cytokines. This report focuses on functional polymorphisms in the genes encoding for several cytokines involved in the pathogenesis of contact allergic responses, including tumour necrosis factor (TNF)-alpha (G-238 A, G-308 A), interleukin (IL)-1beta (C-511G, T+ 3953C), its natural antagonist, the IL-1 receptor antagonist (VNTR intron 2), and IL-6 (G-174C). Polymorphisms were investigated by PCR techniques among polysensitized individuals, defined as individuals with confirmed contact sensitization to para-substituted aryl compounds and at least one other structurally unrelated allergen (n = 86), and healthy control individuals without a history of eczema (n = 310). The distribution of TNFA-308 genotypes was significantly different in these groups (Padjusted= 0.0378). Compared with carriers of 2 wild-type alleles (TNFA-308*1/1 (*G/G)), carriers of the TNFA-308*1/2 (*G/A) and TNFA-308*2/2 (*A/A) genotypes tended to be more common among polysensitized individuals [OR = 1.54, 95% CI (0.92-2.55) and OR = 2.36 (0.84-6.51), respectively]. No significantly different distribution of genotypes was detected at any other polymorphic loci among control individuals without eczema and polysensitized subjects. These findings suggest a possible relationship between the TNFA-308 polymorphism and contact allergy. The results need to be confirmed in future studies.

Publication types

  • Clinical Trial
  • Comparative Study
  • Controlled Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age Distribution
  • Alleles
  • Austria / epidemiology
  • Case-Control Studies
  • Cytokines / genetics
  • Dermatitis, Allergic Contact / epidemiology
  • Dermatitis, Allergic Contact / genetics*
  • Dermatitis, Atopic / diagnosis
  • Dermatitis, Atopic / epidemiology
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease*
  • Genotype
  • Humans
  • Incidence
  • Interleukin-1 / analysis
  • Male
  • Middle Aged
  • Polymorphism, Genetic*
  • Probability
  • Receptors, Interleukin-1 / genetics
  • Reference Values
  • Sex Distribution
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • Cytokines
  • Interleukin-1
  • Receptors, Interleukin-1
  • Tumor Necrosis Factor-alpha