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The −431C>T polymorphism of thymus and activation‐regulated chemokine increases the promoter activity but is not associated with susceptibility to atopic dermatitis in Japanese patients
Author(s) -
Tsunemi Yuichiro,
Komine Mayumi,
Sekiya Takashi,
Saeki Hidehisa,
Nakamura Koichiro,
Hirai Koichi,
Kakinuma Takashi,
Kagami Shinji,
Fujita Hideki,
Asano Noriko,
Tanida Yuka,
Wakugawa Motoshi,
Torii Hideshi,
Tamaki Kunihiko
Publication year - 2004
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2004.00225.x
Subject(s) - single nucleotide polymorphism , genotype , allele , snp , atopic dermatitis , promoter , microbiology and biotechnology , chemokine , gene , biology , immunology , allele frequency , genetics , gene expression , inflammation
Background: Thymus and activation‐regulated chemokine (TARC) plays an important role in the pathogenesis of atopic dermatitis (AD). We recently detected the single nucleotide polymorphism (SNP) (−431C>T) in the 5′‐flanking region of TARC gene. Objectives: To examine whether the −431C>T SNP of the TARC gene is associated with susceptibility to AD and whether it affects the promoter activity of the TARC gene. Methods: We investigated the genotype and allele frequencies of the SNP in 193 AD patients and 158 healthy controls by polymerase chain reaction‐restriction fragment length polymorphism method. We compared the promoter activities between TARC promoter carrying 431C and that carrying −431T by transient‐transfection assay in DJM‐1 cell line. Results: There were no significant differences in genotype or allele frequencies between AD patients and controls (genotype: P = 0.38, allele: P = 0.22). Luciferase activity was higher in −431T constructs than in −431C constructs (2.3‐fold, P = 9.5 × 10 −6 ). Conclusion: These results suggest that the −431C>T SNP of the TARC gene enhances the promoter activity of TARC gene but is not associated with susceptibility to AD in Japanese population.