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首页> 外文期刊>Cytokine >TNF-alpha levels are not increased in inflamed patients carrying the CCR5 deletion 32.
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TNF-alpha levels are not increased in inflamed patients carrying the CCR5 deletion 32.

机译:在患有CCR5缺失的发炎患者中,TNF-α水平并未增加32。

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BACKGROUND AND AIMS: Recently we reported on a genetically predisposed protection from C-reactive protein (CRP) related mortality in dialysis patients carrying the functional CC-chemokine receptor 5 deletion 32 allele (CCR5Delta32) mutation. Since CCR5Delta32 is associated with a less pro-inflammatory immune response in mice, we hypothesized that the observed protection is (in part) due to a less pro-inflammatory cytokine profile. METHODS: Cross-sectional observational study including 263 incident dialysis patients aged 18-70years, without clinical signs of infection and/or acute vasculitis. TNF-alpha, IL-6, IL-10 and hsCRP levels were determined and studied in relation to the CCR5 genotype. RESULTS: In the presence of elevated hsCRP, IL-6 concentration was higher irrespective of the CCR5 genotype. However, in patients with the CCR5 deletion, TNF-alpha did not differ in the presence/absence of elevated hsCRP and was not correlated with hsCRP levels in carriers of the CCR5Delta32 polymorphism. CONCLUSIONS: A possible underlying mechanism of the impact of CCR5Delta32 genotype on inflammation driven mortality in dialysis patients could be a reduced Th1 immune response as represented by decreased TNF-alpha levels.
机译:背景与目的:最近,我们报道了携带功能性CC趋化因子受体5缺失32等位基因(CCR5Delta32)突变的透析患者对C反应蛋白(CRP)相关死亡率的遗传易感性保护作用。由于CCR5Delta32与小鼠体内较少的促炎性免疫反应相关,因此我们假设观察到的保护作用(部分)是由于较少的促炎性细胞因子引起的。方法:横断面观察性研究包括263名年龄在18-70岁之间,没有感染和/或急性血管炎临床症状的透析患者。确定和研究与CCR5基因型相关的TNF-α,IL-6,IL-10和hsCRP水平。结果:在高hsCRP的存在下,IL-6浓度较高,而与CCR5基因型无关。但是,在CCR5缺失的患者中,TNF-α在hsCRP升高与否之间没有差异,并且与CCR5Delta32多态性携带者中的hsCRP水平无关。结论:在透析患者中​​,CCR5Delta32基因型对炎症驱动死亡率影响的可能的潜在机制可能是Th1免疫应答降低,以TNF-α水平降低为代表。

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