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土耳其高安动脉炎患者白细胞介素(IL)-12、IL-2和IL-6基因多态性

Interleukin (IL)-12, IL-2, and IL-6 gene polymorphisms in Takayasu's arteritis from Turkey.

作者信息

Saruhan-Direskeneli G, Biçakçigil M, Yilmaz V, Kamali S, Aksu K, Fresko I, Akkoç N, Kiraz S, Ozer H T E, Tunç E, Yücel E, Karaarslan Y, Uyar F A, Doganavşargil E, Inanc M, Direskeneli H

机构信息

Istanbul University Istanbul Medical Faculty, Department of Physiology, Istanbul, Turkey.

出版信息

Hum Immunol. 2006 Sep;67(9):735-40. doi: 10.1016/j.humimm.2006.06.003. Epub 2006 Jul 20.

Abstract

Takayasu's arteritis (TA) is a chronic arterial inflammation of unknown etiology involving mainly the aorta and its major branches. Genetic polymorphisms of cytokines are screened as susceptibility factors for TA in Turkey. A total of 94 patients with TA were investigated for the genetic polymorphisms of the interleukin genes IL12, IL2,and IL6 and were compared with 108 healthy control subjects using polymerase chain reaction-sequence-specific primer method. The frequencies of IL12B 1188 C allele (p = 0.03, OR = 1.7) and CC genotype (p = 0.007, OR = 3.7) were both higher in TA patients than in control subjects. TT genotype at IL2-330 (p = 0.006, OR = 2.4) and GG genotype at IL6-174 (p = 0.04, OR = 1.9) were more frequent in TA patients. Lower prevalence of GT genotype at IL2-330 (p = 0.005, OR = 0.4), CG genotype at IL6-174 (p = 0.001, OR = 0.4), and AG genotypes at IL6-598 (p = 0.01, OR = 0.4) were also detected. The polymorphism of IL-12 as well as IL-6 and IL-2 genes may contribute to susceptibility and pathogenesis of TA by altering cytokine production and inducing inflammation.

摘要

高安动脉炎(TA)是一种病因不明的慢性动脉炎症,主要累及主动脉及其主要分支。在土耳其,细胞因子的基因多态性被筛查为TA的易感因素。共对94例TA患者进行白细胞介素基因IL12、IL2和IL6的基因多态性研究,并采用聚合酶链反应-序列特异性引物法与108名健康对照者进行比较。TA患者中IL12B 1188 C等位基因频率(p = 0.03,OR = 1.7)和CC基因型频率(p = 0.007,OR = 3.7)均高于对照组。TA患者中IL2 - 330位点的TT基因型(p = 0.006,OR = 2.4)和IL6 - 174位点的GG基因型(p = 0.04,OR = 1.9)更为常见。还检测到IL2 - 330位点GT基因型(p = 0.005,OR = 0.4)、IL6 - 174位点CG基因型(p = 0.001,OR = 0.4)和IL6 - 598位点AG基因型(p = 0.01,OR = 0.4)的患病率较低。IL - 12以及IL - 6和IL - 2基因的多态性可能通过改变细胞因子产生和诱导炎症而导致TA的易感性和发病机制。

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