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Allelic variants of CD40 and CD40L genes interact to promote antibiotic-induced cutaneous allergic reactions

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dc.contributor.authorKim, Sae-H-
dc.contributor.authorLee, J-E-
dc.contributor.authorKim, Sang-H-
dc.contributor.authorJee, Y-K-
dc.contributor.authorPark, H-S-
dc.contributor.authorPark, H-W-
dc.contributor.authorMin, K-U-
dc.contributor.authorKim, Y-K-
dc.date.accessioned2012-05-23T04:26:02Z-
dc.date.available2012-05-23T04:26:02Z-
dc.date.issued2009-12-
dc.identifier.citationCLINICAL AND EXPERIMENTAL ALLERGY; Vol.39 12; 1852-1856ko_KR
dc.identifier.issn0954-7894-
dc.identifier.urihttps://hdl.handle.net/10371/76318-
dc.description.abstractP>Background The danger hypothesis provides a new perspective of the mechanisms underlying drug allergy. In this study, we evaluated associations between variations in the genes involved in danger signal pathways and antibiotic-induced cutaneous allergic reactions (AICARs). Methods Two hundred cases with urticaria, angio-oedema, maculopapular rash, and erythema multiforme caused by antibiotics were extracted from the database of the Adverse Drug Reaction Research Group in Korea. All cases were confirmed by an allergy specialist. Causative antibiotics included penicillin, cephalosporin, quinolone, and others (approximately 40 different types). Ten single nucleotide polymorphisms (SNPs) in seven genes (-318C > T, +49A > G, and +6230G > A in CTLA4, IVS+17T > C in CD28, -3479T > G and I170V in CD86, -1C > T in CD40, -3458A > G in CD40LG, -308G > A in TNF, and -31T > C in IL1B) were scored for cases and for healthy subjects without a history of AICARs. Results Our analysis failed to reveal differences in the distribution of the 10 SNPs between cases and controls. However, we could find a gene-gene interaction between -1C > T in CD40 and -3458A > G in CD40L using multifactor dimensionality reduction analysis. Subjects with minor alleles of both SNPs showed a significant risk for developing AICARs [P=0.017, odds ratio (OR) (95% confidence interval)=2.93 (1.20-7.97)]. Conclusion Our findings suggest that a genetic interaction between CD40 and CD40L favours the development of AICARs. Cite this as: Sae-H Kim, J-E Lee, Sang-H Kim, Y-K Jee, Y-K Kim, H-S Park, K-U Min, H-W Park and The Adverse Drug Reaction Research Group in Korea, Clinical & Experimental Allergy, 2009 (39) 1852-1856.ko_KR
dc.language.isoenko_KR
dc.publisherWILEY-BLACKWELL PUBLISHING, INCko_KR
dc.subjectantibioticsko_KR
dc.subjectdrug hypersensitivityko_KR
dc.subjectCD40ko_KR
dc.subjectCD40 ligandko_KR
dc.titleAllelic variants of CD40 and CD40L genes interact to promote antibiotic-induced cutaneous allergic reactionsko_KR
dc.typeArticleko_KR
dc.identifier.doi10.1111/j.1365-2222.2009.03336.x-
dc.citation.journaltitleCLINICAL AND EXPERIMENTAL ALLERGY-
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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