title: Cytokine gene polymorphisms in allergic contact dermatitis.
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.
authors.affiliation: Department of Occupational Health, Georg-August-University, Göttingen, Germany. gwestph@gwdg.de
authors.forename: Götz A
authors.initials: GA
authors.lastname: Westphal
authors.forename: Axel
authors.initials: A
authors.lastname: Schnuch
authors.forename: Rotraut
authors.initials: R
authors.lastname: Moessner
authors.forename: Inke R
authors.initials: IR
authors.lastname: König
authors.forename: Birger
authors.initials: B
authors.lastname: Kränke
authors.forename: Ernst
authors.initials: E
authors.lastname: Hallier
authors.forename: Andreas
authors.initials: A
authors.lastname: Ziegler
authors.forename: Kristian
authors.initials: K
authors.lastname: Reich
mesh_terms: D000328:Adult; D017677:Age Distribution; D000483:Alleles; D001317:Austria / Q000453:epidemiology; D016022:Case-Control Studies; D016207:Cytokines / Q000235:genetics; D017449:Dermatitis, Allergic Contact / Q000453:epidemiology / Q000235:genetics*; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000453:epidemiology; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D015994:Incidence; D007375:Interleukin-1 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011336:Probability; D017472:Receptors, Interleukin-1 / Q000235:genetics; D012016:Reference Values; D017678:Sex Distribution; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha