Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Anhui, PR China.
Lupus. 2011 Aug;20(9):945-51. doi: 10.1177/0961203311400114. Epub 2011 Jun 2.
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.
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.
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.
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.
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。
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。
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。
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。