Single nucleotide polymorphisms in the tumor necrosis factor-alpha gene promoter region alter the risk of psoriasis vulgaris and psoriatic arthritis: a meta-analysis.
Single nucleotide polymorphisms in the tumor necrosis factor-alpha gene promoter region alter the risk of psoriasis vulgaris and psoriatic arthritis: a meta-analysis.
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肿瘤坏死因子-α 基因启动子区的单核苷酸多态性改变寻常型银屑病和银屑病关节炎的风险：荟萃分析
DOI：
10.1371/journal.pone.0064376
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Li J
中科院分区：
文献类型：
--
作者：
Zhu J;Qu H;Chen X;Wang H;Li J
肿瘤坏死因子α（TNFα）是一种巨噬细胞源性的促炎细胞因子，在寻常型银屑病和银屑病关节炎（PsV&PsA）的发病机制中起重要作用。与此相反，TNFα基因启动子区单核苷酸多态性（SNPs）与PsV和PsA之间的关系仍存在争议。因此，我们进行了一项荟萃分析，以提供新的证据表明，TNFα基因启动子区的SNP不仅改变寻常型银屑病（PsV）或银屑病关节炎（PsA）的风险，而且还改变PsV和PsA的风险。从PubMed、ScienceDirect和SpringerLink数据库中获取了日期为2012年10月的相关文献。获得了PsV和PsA以及对照受试者中TNFα启动子的基因型和/或等位基因的数量。采用比值比（OR）和95%置信区间（CI）计算TNFα启动子SNP的PsV和/或PsA风险。共纳入26篇关于PsV（2129名正常对照）和PsA（2997名正常对照）的2159篇论文。结果表明，TNFα -308A/G基因型和等位基因在PsV和PsA合并组中具有保护作用（OR = 0.682，0.750; 95% CI为0.596-0.779，0.653-0.861）。 TNFα -238A/G和-857T/C基因型和等位基因变异与PsV和PsA的发病风险相关（OR = 2.493，2.228，1.536，1.486，95% CI，1.777-3.498，1.628-3.049，1.336-1.767，1.309-1.685）。 Meta分析显示TNFα -238A/G和-857T/C多态性与PsA易感性显著相关（OR = 2.242，2.052，1.419，1.465; 95%CI，1.710-2.941，1.614-2.610，1.214-1.658，1.277-1.681）。 TNFα -308A/G基因型和等位基因对PsV具有保护作用（OR = 0.574，0.650，95% CI，0.478-0.690，0.556-0.759），而TNFα -238A/G基因型和等位基因与PsV的发病风险相关（OR = 2.636，2.223，95% CI，1.523-4.561，1.317-3.751）。 TNFα基因启动子区的SNP改变了PsV和/或PsA的风险。
It has been confirmed that tumor necrosis factor-alpha (TNFα), a macrophage-derived pro-inflammatory cytokine, plays an important role in the pathogenesis of psoriasis vulgaris and psoriatic arthritis (PsV&PsA). In contrast, the reported association of TNFα gene promoter region single nucleotide polymorphisms (SNPs) and PsV&PsA has remained controversial. Accordingly, we performed a meta-analysis to provide new evidence that SNPs in the TNFα gene promoter region alter not only the risk of psoriasis vulgaris (PsV) or psoriatic arthritis (PsA) but also of PsV&PsA. Interrelated literature dated to October 2012 was acquired from the PubMed, ScienceDirect, and SpringerLink databases. The number of the genotypes and/or alleles for the TNFα promoter in the PsV and PsA and control subjects was obtained. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to calculate the risk of PsV and/or PsA with TNFα promoter SNPs. A total of 26 papers of 2159 for PsV (2129 normal controls) and 2360 for PsA (2997 normal controls) were included in our meta-analysis. The results showed that the variant genotype and allele of TNFα -308A/G was protective in pooled groups of patients with PsV&PsA (OR = 0.682, 0.750; 95% CI, 0.596-0.779, 0.653-0.861). However, the variant genotypes and alleles of TNFα -238A/G and -857T/C had an increased risk of PsV&PsA (OR = 2.493, 2.228, 1.536, 1.486, 95% CI, 1.777-3.498, 1.628-3.049, 1.336-1.767, 1.309-1.685). Moreover, the meta-analysis revealed a significant association between TNFα -238A/G and -857T/C polymorphism and PsA susceptibility (OR = 2.242, 2.052, 1.419, 1.465; 95% CI, 1.710-2.941, 1.614-2.610, 1.214-1.658, 1.277-1.681). In contrast, the variant genotypes and alleles of TNFα -308A/G proved to be protective against PsV (OR = 0.574, 0.650, 95% CI, 0.478-0.690, 0.556-0.759), whereas TNFα -238A/G was found to have a risk association (OR = 2.636, 2.223, 95% CI, 1.523-4.561, 1.317-3.751). SNPs in the TNFα gene promoter region alter the risk of PsV and/or PsA.
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