Influence of TNF and IL10 gene polymorphisms in the immunopathogenesis of leprosy in the south of Brazil

Influence of TNF and IL10 gene polymorphisms in the immunopathogenesis of leprosy in the south of Brazil
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DOI:
10.1016/j.ijid.2008.08.019
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发表时间:
2009-07-01
影响因子:
8.4
通讯作者:
Laguila Visentainer, Jeane Eliete
Laguila Visentainer, Jeane Eliete
中科院分区:
医学2区
文献类型:
--
作者:
Alessio Franceschi, Danilo Santana;Mazini, Priscila Saamara;Laguila Visentainer, Jeane Eliete

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目的:为了确定是否细胞因子多态性与麻风和/或其亚型在巴西population.Methods:基因分型使用聚合酶链反应与序列特异性引物(PCR-SSP)进行:TNF-308/-238 IL 2(-330/+166)、IL6(-174)、IFNG(+874)、TGFB1(+869/+915)和IL 10(-592/-819/-1082)。对于TNF-308,GG基因型的频率较高,(85.5%vs.74.1%,p = 0.009),与对照组相比,麻风患者中GA/AA基因型频率沿着降低(14.5%对比25.9%,p = 0.009)。GG基因型在类结核型(TT)和交界型(BB)麻风患者中尤其高(分别为90.5%和89.8%)。IL 10基因型分析显示,瘤型麻风(LL)患者中GCC/GCC单倍型的频率(6.2%)低于对照组(15.4%)。结论:TNF启动子区-308位点G-> A置换在麻风发病中起重要作用。(C)2008年国际传染病学会。由爱思唯尔有限公司出版。保留所有权利。
Objective: To determine whether cytokine polymorphisms are associated with leprosy and/or their subtypes in a Brazilian population.Methods: Genotyping using polymerase chain reaction with sequence-specific primers (PCR-SSP) was performed for: TNF-308/-238 IL2(-330/+166), IL6(-174), IFNG(+874), TGFB1(+869/+915) and IL 10(-592/-819/-1082) in 240 healthy controls and 167 patients with leprosy.Results: For TNF-308, a higher frequency of GG genotype (85.5% vs. 74.1% in healthy controls, p = 0.009), along with a decreased frequency of GA/AA genotypes was observed among leprosy patients as compared to the control group (14.5% vs. 25.9%, p = 0.009). The GG genotype was particularly higher in patients with tuberculoid (TT) and borderline (BB) leprosy (90.5% and 89.8%, respectively). Analysis of IL10 genotypes revealed a lower frequency of GCC/GCC haplotype in lepromatous leprosy (LL) patients (6.2%) in comparison to controls (15.4%).Conclusion: It is suggested that the G -> A substitution at position -308 in the TNF promoter region plays an important role in leprosy patients. (C) 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.