A TNFR2 3' flanking region polymorphism in systemic lupus erythematosus.

A TNFR2 3' flanking region polymorphism in systemic lupus erythematosus.
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系统性红斑狼疮中的 TNFR2 3 侧翼区域多态性。

DOI:
10.1038/sj.gene.6363662
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发表时间:
2000
期刊:
影响因子:
5
通讯作者:
Petri,MA
Petri,MA
中科院分区:
医学3区
文献类型:
--
作者:
Sullivan,KE;Piliero,LM;Goldman,D;Petri,MA

文献摘要

被引文献

相似文献

促炎细胞因子在系统性红斑狼疮(SLE)中的作用仍存在一定争议。一些研究表明SLE患者TNFα和IL-6的产生增加。还报告了IL-6、TNFα和IL-1可溶性受体的产生增加。这一发现是挑衅性的,因为可溶性受体有能力作为拮抗剂。其他几种炎症性疾病也与可溶性TNFα受体的产生增加相关,表明这可能是一种旨在下调炎症的一般代偿机制。最近发现的SLE疾病易感性基因座附近的TNFR 2基因座(TNFR p75)建议的假设,遗传驱动的差异,可溶性TNFR 2的生产可以发挥作用的遗传易感性SLE。因此,我们对白种人SLE患者和地理位置匹配的对照组中TNFR 2基因3′非翻译区的遗传多态性频率进行了表征。与对照组相比,SLE患者的两个碱基对多态性的基因频率没有差异,也没有发现与任何特定的临床表型有任何关联。
The role of pro-inflammatory cytokines in systemic lupus erythematosus (SLE) remains somewhat controversial. Several studies have shown increased production of TNFα and IL-6 in patients with SLE. Increased production of IL-6, TNFα, and IL-1 soluble receptors have also been reported. This finding is provocative because the soluble receptors have the capacity to act as antagonists. Several other inflammatory disorders are also associated with increased production of soluble TNFα receptors suggesting that this may be a general compensatory mechanism designed to down-regulate inflammation. The recent identification of an SLE disease susceptibility locus near the TNFR2 locus (TNFR p75) suggested the hypothesis that genetically driven differences in soluble TNFR2 production could play a role in the genetic susceptibility to SLE. We therefore characterized the frequency of a genetic polymorphism in the 3′ untranslated region of the TNFR2 gene in Caucasoid SLE patients and geographically matched controls. No difference in the gene frequency of the two base-pair polymorphism in SLE patients compared to controls was found, nor was there any association with any particular clinical phenotype.