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首页> 外文期刊>Clinical and experimental allergy : >Allelic variants of CD40 and CD40L genes interact to promote antibiotic-induced cutaneous allergic reactions.
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Allelic variants of CD40 and CD40L genes interact to promote antibiotic-induced cutaneous allergic reactions.

机译：CD40和CD40L基因的等位基因变体相互作用以促进抗生素诱导的皮肤过敏反应。

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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.
机译：背景：危险假设为药物过敏的潜在机制提供了新的视角。在这项研究中，我们评估了危险信号通路中涉及的基因变异与抗生素诱导的皮肤过敏反应（AICAR）之间的关联。方法：从韩国药物不良反应研究小组的数据库中提取了200例由抗生素引起的荨麻疹，血管性水肿，斑丘疹和多形性红斑的病例。所有病例均经过敏专家确认。致病性抗生素包括青霉素，头孢菌素，喹诺酮等（约40种不同类型）。 CTLA4中的七个基因（-318C> T，+ 49A> G和+ 6230G> A，CD28中的IVS + 17T> C，CD86中的-3479T> G和I170V，十个单核苷酸多态性（SNPs），-1C> T在病例中和没有AICAR病史的健康受试者中，对CD40中的-3458A> G，CD40LG中的-3458A> G，TNF中的-308G> A和IL1B中的-31T> C进行评分。结果：我们的分析未能揭示病例与对照之间10个SNPs分布的差异。然而，使用多维度降维分析，我们可以发现CD40中的-1C> T与CD40L中的-3458A> G之间存在基因-基因相互作用。两个SNPs等位基因均较小的受试者显示出显着发展AICAR的风险[P = 0.017，优势比（OR）（95％置信区间）= 2.93（1.20-7.97）]。结论：我们的发现表明CD40和CD40L之间的遗传相互作用有利于AICAR的发展。

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