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

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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-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.

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Correspondence to Ayca Cordan Yazici.

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Yazici, A.C., Erdal, M.E., Kaya, T.I. et al. Lack of association with TNF-α-308 promoter polymorphism in patients with vitiligo. Arch Dermatol Res 298, 46–49 (2006). https://doi.org/10.1007/s00403-006-0664-2

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  • DOI: https://doi.org/10.1007/s00403-006-0664-2

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