title: Lack of association with TNF-alpha-308 promoter polymorphism in patients with vitiligo.
abstract: Vitiligo is an acquired depigmentary disorder of the skin, characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. An immunologic hypothesis is currently advanced as a possible pathogenesis of vitiligo. The cytokines have an important role in pathogenesis of autoimmunity in which tumor necrosis factor-alpha (TNF-alpha), a paracrine inhibitor of melanocytes, is especially important. Several single-nucleotide polymorphisms (SNP) have been identified in the human TNF gene promoter. The polymorphism at position -308 (TNF-308), which involves substituting G for A and designing the AA genotype, leads to a higher rate of TNF gene transcription than the wild-type GG genotype in in vitro expression studies. It has also been linked to increased susceptibility to several chronic metabolic, degenerative, inflammatory and autoimmune diseases. Therefore, we investigated the TNF-alpha-308 SNP in patients with vitiligo. We examined 61 patients with vitiligo. Healthy age-, ethnically- and sex-matched individuals (n = 123) served as controls. Polymerase chain reaction amplification was used for analysis of the polymorphism at position -308 in promoter of TNF-alpha gene. We found that the distribution of TNF-alpha genotypes in vitiligo patients did not differ from that in control subjects (P > 0.05). Moreover, there was no association between TNF-alpha genotypes and types of vitiligo. In conclusion, we suggest that TNF-alpha-308 SNP is not a genetic risk factor for vitiligo susceptibility.
authors.affiliation: Department of Dermatology, School of Medicine, Mersin University, 33079 Mersin, Turkey. aycacordan@yahoo.com
authors.forename: Ayca Cordan
authors.initials: AC
authors.lastname: Yazici
authors.forename: M Emin
authors.initials: ME
authors.lastname: Erdal
authors.forename: Tamer Irfan
authors.initials: TI
authors.lastname: Kaya
authors.forename: Guliz
authors.initials: G
authors.lastname: Ikizoglu
authors.forename: Kaan
authors.initials: K
authors.lastname: Savasoglu
authors.forename: Handan
authors.initials: H
authors.lastname: Camdeviren
authors.forename: Umit
authors.initials: U
authors.lastname: Tursen
mesh_terms: D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D014820:Vitiligo / Q000235:genetics*
chemical_list: D014409:Tumor Necrosis Factor-alpha