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J Invest Dermatol. 2004 Jan;122(1):87-94.

Tumor necrosis factor-alpha and interferon-gamma polymorphisms contribute to susceptibility to oral lichen planus.

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1
Department of Biomedical Sciences and Human Oncology, Oral Medicine Section, School of Medicine and Dentistry, University of Turin, Italy. carrozzo@unito.it

Erratum in

  • J Invest Dermatol. 2004 Oct;123(4):805.

Abstract

Most lymphocytes in the lamina propria of oral lichen planus (OLP) lesions express and secrete interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), whereas they do not secret interleukin-4 and -10 or transforming growth factor-beta. We analyzed whether the polymorphisms of several cytokines may influence the susceptibility to OLP. Cytokine typing was performed by a sequence-specific PCR assay. Thirteen cytokine genes with 22 single-nucleotide polymorphisms were studied. IFN-gamma UTR 5644 genotype frequencies showed a significant increase in number of T/T homozygotes in OLP patients compared with controls (40.9 vs. 22.9%; p=0.0022). Moreover, in OLP patients, the frequency of the -308A TNF-alpha allele was higher than in the controls (21.6 vs. 9.3%; p < 0.05) causing a significantly increased frequency of the genotype G/A in OLP (43.2 vs. 14.3%; p=0.0002). Because in patients with mucocutaneous lichen planus (LP), the frequency of the -308A TNF-alpha allele was more than double the values in the pure OLP patients (40.9 vs. 15.1%; p=0.003), the -308G/A TNF-alpha genotype showed a significantly higher frequency in patients with mucocutaneous LP than in patients with pure OLP (81.8 vs. 30.3%, p=0.003). In conclusion, we suggest that genetic polymorphism of the first intron of the promoter gene of IFN-gamma may be an important risk factor to develop oral lesions of LP, whereas an increase in the frequency of -308A TNF-alpha allele may best contribute to the development of additional skin involvement.

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