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首页> 外文期刊>International journal of immunogenetics >Association of -308 TNF-alpha promoter polymorphism with type 1 diabetes in North Indians.
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Association of -308 TNF-alpha promoter polymorphism with type 1 diabetes in North Indians.

机译：-308TNF-α启动子多态性与北印度人的1型糖尿病的关联。

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摘要

Tumour necrosis factor alpha (TNF-alpha) is a pleiotropic cytokine with a potent immunomodulatory activity. In humans, TNF-alpha gene is located on chromosome 6p21.31 in the region of highly polymorphic human leucocyte antigen (HLA) gene complex, hence the genetic variability of TNF-alpha has been widely implicated in the altered expression of the gene leading to different inflammatory conditions and autoimmune diseases including type 1 diabetes. We assessed the association of TNF-alpha promoter polymorphisms at -308 and -23 8 sites with type 1 diabetes and correlated it with TNF-alpha production in the serum and by the lipopolysaccharide-activated peripheral blood mononuclear cells in North Indian subjects. Genotyping was performed on 130 patients and 133 normal subjects by polymerase chain reaction-restriction fragment length polymorphism analysis using NcoI and BglII restriction endonucleases. The frequency of A allele and AG genotype at -308 site was significantly higher in patients with type 1 diabetes than that of the controls (P_c = 0.000248 and 0.000438, respectively) while no significant difference was observed at -238 site between the two groups. The frequency of A allele at -238 site was very rare (< 2%) among the patients and was absent in the control group. The AG genotype at -308 site was associated with relatively higher production of TNF-alpha in the peripheral blood (P < 0.001), as well as by the peripheral blood mononuclear cells both at the basal level (P < 0.05) and after stimulation with lipopolysaccharide as compared to the -308 GG genotype. The results of the present study suggest that higher frequency of A allele at the -308 promoter site may be related to higher expression of TNF-alpha gene consequently leading to increased susceptibility to type 1 diabetes in North Indians.
机译：肿瘤坏死因子α（TNF-alpha）是一种具有有效免疫调节活性的多效性细胞因子。在人类中，TNF-α基因位于高度多态性人类白细胞抗原（HLA）基因复合体区域的6p21.31号染色体上，因此TNF-α的遗传变异性已广泛涉及该基因的表达改变，从而导致不同的炎症和自身免疫性疾病，包括1型糖尿病。我们评估了在-308和-23 8位点的TNF-α启动子多态性与1型糖尿病的关联，并将其与血清中TNF-α的产生以及在北印度受试者中脂多糖激活的外周血单核细胞的相关性。通过使用NcoI和BglII限制性核酸内切酶的聚合酶链反应-限制性片段长度多态性分析，对130例患者和133名正常受试者进行了基因分型。 1型糖尿病患者在-308位点的A等位基因和AG基因型的频率显着高于对照组（分别为P_c = 0.000248和0.000438），而两组之间在-238位点没有显着差异。在患者中，-238位点的A等位基因频率非常罕见（<2％），而在对照组中则没有。在-308位点的AG基因型与外周血中相对较高的TNF-α产量相关（P <0.001），以及在基础水平（P <0.05）以及经H2O2刺激后的外周血单核细胞。脂多糖与-308 GG基因型相比。本研究的结果表明，-308启动子位点A等位基因频率较高可能与TNF-α基因的较高表达有关，从而导致北印度人对1型糖尿病的敏感性增加。

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