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首页> 外文期刊>Journal of genetics >Genetic and expression changes in TNF-?± as a risk factor for rheumatoid arthritis pathogenesis in northeast India
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Genetic and expression changes in TNF-?± as a risk factor for rheumatoid arthritis pathogenesis in northeast India

机译：遗传和表达在TNF-？±作为印度东北部的类风湿性关节炎发病机制的危险因素

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Antitumour necrosis factor-alpha (TNF-?±) therapy is used as a clinical intervention for rheumatoid arthritis (RA) but differences exist in response to the treatment which makes the candidature of the screening of TNF-?± alteration(s) at genetic and expression levels an important agenda prior to treatment. This study aims to determine the associative role of TNF-?± a??308G/A polymorphism and differential expression of TNF-?± in the pathogenesis of RA. A casea??control study where a total of 126 RA patients were enrolled based on ACR-EULAR (2010) criteria, along with 160 community matched age and sex controls over a period of three years. The differential expression level of TNF-?± mRNA and protein level was studied and TNF-?± a??308G/A polymorphism was screened by T-ARMS PCR assay. All statistical analysis was performed using SPSS software. mRNA expression level of TNF-?± was upregulated in RA cases (avg. 15.85 ?± 9.52 fold) compared to control. TNF-?± protein level was found to be higher in RA cases (28.62?±7.17 pg/mL) compared to control (23.14?±6.91 pg/mL). TNF-?± a??308 variant GA genotype was higher in RA (46.03%) than in control (25%). The presence of TNF-?± a??308 variant A allele was associated with increased risk of RA susceptibility (odds ratio (OR) = 2.559 at 95% confidence interval (CI), P 0.001) but not severity (OR = 1.617 at 95% CI, P = 0.571). The presence of a??308 variant genotype was associated with a higher TNF-?± mRNA and protein expression. The presence of TNF-?± a??308A allele is associated with increased risk of RA susceptibility and differential TNF-?± expression, and has prognostic significance. Association of higher TNF-?± pro-inflammatory cytokine levels with northeast Indian patients makes them suitable subjects for anti-TNF-?± therapy.
机译：抗肿瘤坏死因子-α（TNF-α±）治疗用作类风湿性关节炎（RA）的临床干预，但响应于治疗的差异存在于遗传术中筛选TNF-α±改变的候选和表达水平治疗前的重要议程。本研究旨在确定TNF-α的关联作用308g / a ?? 308g / a多态性和TNF-β±差异在Ra的发病机制中的差异表达。一个卡西亚的对照研究，基于ACR-euary（2010）标准，共有126名RA患者，以及160个社区匹配年龄和性别控制，在三年内。研究了TNF-α±mRNA和蛋白质水平的差异表达水平，并通过T臂PCR测定筛选308g /ααααααααααααβ。使用SPSS软件进行所有统计分析。与对照相比，在RA病例（AVG。15.85±9.52倍）中上调TNF-α±mRNA表达水平。与对照（23.14±6.91pg / ml）相比，RNF-α蛋白水平在RA病例（28.62〜±7.17 pg / ml）中较高。 TNF-？±A ?? 308变体GA基因型在Ra（46.03％）中高于对照（25％）。 TNF-αααα的存在308变体与Ra易感性的风险增加有关（在95％置信区间（CI），P <0.001）但不严重程度（或= 1.617）的增加有关（OR）= 2.559的风险增加在95％CI，P = 0.571）。存在308个变体基因型的存在与较高的TNF-α±mRNA和蛋白质表达有关。 TNF-α±a ?? 308a等位基因的存在与RA易感性和差异TNF-α±表达的风险增加有关，并且具有预后意义。与东北印度患者的较高TNF-α-炎症细胞因子水平的关联使其适用于抗TNF-α±疗法的受试者。

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