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肿瘤坏死因子-α -308A与白细胞介素-10 -1082G基因多态性及相关细胞因子血清水平升高的联合作用:白癜风易感性

The combination of tumour necrosis factor-α -308A and interleukin-10 -1082G gene polymorphisms and increased serum levels of related cytokines: susceptibility to vitiligo.

作者信息

Aydıngöz I E, Kanmaz-Özer M, Gedikbaşi A, Vural P, Doğru-Abbasoğlu S, Uysal M

机构信息

Department of Dermatology, School of Medicine, Acibadem University, Istanbul, Turkey.

出版信息

Clin Exp Dermatol. 2015 Jan;40(1):71-7. doi: 10.1111/ced.12446. Epub 2014 Oct 4.

Abstract

BACKGROUND

The aetiopathogenesis of vitiligo is still under investigation.

AIM

To assess the role of single nucleotide polymorphisms (SNPs) of the genes for tumour necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10, as well as the serum levels of these three cytokines in the pathogenesis of vitiligo.

METHODS

The study enrolled 105 patients with vitiligo, and 211 age- and sex-matched controls. TNF-α (-308), IL-6 (-174) and IL-10 (-1082) promoter polymorphisms were investigated by LightSNiP assay and analysed by χ(2) test. Subsequently, the serum cytokine levels were assessed by ELISA and evaluated by Mann-Whitney U-test and Kruskal-Wallis test.

RESULTS

The frequency of the GG genotype of the IL-10 -1082 polymorphism was significantly higher in the vitiligo group compared with the healthy control group (P = 0.02). Further investigations using combinations of these variant alleles detected a significant risk for vitiligo for individuals carrying both the IL-10 -1082G and TNF-α -308A alleles (OR = 12.57, 95% CI 1.44-110.0, P < 0.01). Serum IL-10 and TNF-α levels were higher in the vitiligo group (P = 0.001). In addition, TNF-α levels in patients with active disease were significantly higher than in patients with stable disease (P < 0.02).

CONCLUSIONS

The concomitant presence of IL-10 -1082G and TNF-α -308A alleles significantly raises the risk for vitiligo. Furthermore, in accordance with these findings, serum IL-10 and TNF-α were also increased in this study, confirming the role of these cytokines in the pathogenesis of vitiligo.

摘要

背景

白癜风的病因发病机制仍在研究中。

目的

评估肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和IL-10基因的单核苷酸多态性(SNP)以及这三种细胞因子的血清水平在白癜风发病机制中的作用。

方法

该研究纳入了105例白癜风患者和211例年龄及性别匹配的对照。通过LightSNiP检测法研究TNF-α(-308)、IL-6(-174)和IL-10(-1082)启动子多态性,并通过χ²检验进行分析。随后,通过酶联免疫吸附测定(ELISA)评估血清细胞因子水平,并通过曼-惠特尼U检验和克鲁斯卡尔-沃利斯检验进行评估。

结果

与健康对照组相比,白癜风组中IL-10 -1082多态性的GG基因型频率显著更高(P = 0.02)。使用这些变异等位基因组合进行的进一步研究发现,携带IL-10 -1082G和TNF-α -308A等位基因的个体患白癜风的风险显著增加(比值比[OR] = 12.57,95%置信区间[CI] 1.44 - 110.0,P < 0.01)。白癜风组的血清IL-10和TNF-α水平更高(P = 0.001)。此外,活动期疾病患者的TNF-α水平显著高于稳定期疾病患者(P < 0.02)。

结论

IL-10 -1082G和TNF-α -308A等位基因同时存在会显著增加患白癜风的风险。此外,根据这些发现,本研究中血清IL-10和TNF-α也升高,证实了这些细胞因子在白癜风发病机制中的作用。

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