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白细胞介素-18 基因启动子-607A/C 多态性与自身免疫性疾病易感性的相关性:荟萃分析。

Lack of association of interleukin-18 gene promoter -607 A/C polymorphism with susceptibility to autoimmune diseases: a meta-analysis.

机构信息

Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Anhui, PR China.

出版信息

Lupus. 2011 Aug;20(9):945-51. doi: 10.1177/0961203311400114. Epub 2011 Jun 2.

DOI:10.1177/0961203311400114
PMID:21636628
Abstract

OBJECTIVE

Published data on the association between interleukin (IL)-18 gene promoter -607 A/C polymorphism and autoimmune diseases risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed.

METHODS

A total of 17 studies, including six studies on type 1 diabetes (T1D), four on rheumatoid arthritis (RA), five on systemic lupus erythematosus (SLE), three on Crohn's Disease (CD) and three on ulcerative colitis (UC), were available for the meta-analysis. Meta-analysis was performed for genotypes A/A (recessive effect), genotypes A/A + A/C (dominant effect), and A allele in fixed or random-effects models.

RESULTS

Overall, no significantly elevated autoimmune diseases risk was found in all genetic models when all studies were pooled into the meta-analysis. The overall odds ratios (ORs) and 95% confidence intervals (CIs) for A-allele were T1D (OR = 0.938, 95% CI = 0.757-1.162), RA (OR = 0.759, 95% CI = 0.540-1.067), SLE (OR = 0.858, 95% CI = 0.609-1.208), CD (OR = 1.159, 95% CI = 0.975-1.379) and UC (OR = 1.170, 95% CI = 0.977-1.402), respectively. In the subgroup analysis by ethnicity, there was still no significant association detected in all genetic models.

CONCLUSIONS

To date, there is still not enough evidence to indicate the association of IL-18 gene promoter -607 A/C polymorphism and the development of autoimmune diseases.

摘要

目的

关于白细胞介素(IL)-18 基因启动子-607A/C 多态性与自身免疫性疾病风险之间的关联,已有发表的数据尚无定论。为了更准确地评估这种关系,我们进行了荟萃分析。

方法

共有 17 项研究,包括 6 项 1 型糖尿病(T1D)研究、4 项类风湿关节炎(RA)研究、5 项系统性红斑狼疮(SLE)研究、3 项克罗恩病(CD)研究和 3 项溃疡性结肠炎(UC)研究,可用于荟萃分析。采用固定或随机效应模型,对基因型 A/A(隐性效应)、基因型 A/A+A/C(显性效应)和 A 等位基因进行荟萃分析。

结果

总体而言,当所有研究合并进行荟萃分析时,所有遗传模型均未发现自身免疫性疾病风险显著升高。A 等位基因的总体比值比(OR)和 95%置信区间(CI)分别为 T1D(OR=0.938,95%CI=0.757-1.162)、RA(OR=0.759,95%CI=0.540-1.067)、SLE(OR=0.858,95%CI=0.609-1.208)、CD(OR=1.159,95%CI=0.975-1.379)和 UC(OR=1.170,95%CI=0.977-1.402)。按种族亚组分析,所有遗传模型均未发现显著相关性。

结论

迄今为止,尚无足够证据表明白细胞介素-18 基因启动子-607A/C 多态性与自身免疫性疾病的发生有关。

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