Lack of association with TNF-α-308 promoter polymorphism in patients with vitiligo

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-α (TNF-α), 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-α-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-α gene. We found that the distribution of TNF-α genotypes in vitiligo patients did not differ from that in control subjects (P > 0.05). Moreover, there was no association between TNF-α genotypes and types of vitiligo. In conclusion, we suggest that TNF-α-308 SNP is not a genetic risk factor for vitiligo susceptibility.