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

机译:缺乏白介素-18基因启动子-607 A / C多态性与自身免疫性疾病易感性的关联:一项荟萃分析。

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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.
机译:目的:关于白介素(IL)-18基因启动子-607 A / C多态性与自身免疫性疾病风险之间关系的公开数据尚无定论。为了获得更精确的关系估计,进行了荟萃分析。方法:总共17项研究,包括6项关于1型糖尿病(T1D)的研究,4项关于类风湿性关节炎(RA),5项关于系统性红斑狼疮(SLE),3项关于克罗恩病(CD)以及3项关于溃疡性结肠炎(UC) ),可供进行荟萃分析。对固定或随机效应模型中的基因型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,将所有研究汇总到荟萃分析中后,在所有遗传模型中均未发现自身免疫疾病风险显着升高。 A等位基因的总比值比(OR)和95%置信区间(CIs)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)。在按种族进行的亚组分析中,在所有遗传模型中仍未检测到显着关联。结论:迄今为止,仍然没有足够的证据表明IL-18基因启动子-607 A / C多态性与自身免疫性疾病的发展有关。

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