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慢性丙型肝炎病毒感染中CD4+ CD25+ FoxP3+调节性T细胞的扩增。

Expansion of CD4+ CD25+ FoxP3+ regulatory T cells in chronic hepatitis C virus infection.

作者信息

Hashempoor Tayebeh, Bamdad Taravat, Merat Shahin, Janzamin Ehsan, Nemati Leila, Jabbari Hossain, Sharifi Amir-Houshang, Zamini Hediyeh

机构信息

Department of Virology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran, e-mail:

出版信息

Iran J Immunol. 2010 Sep;7(3):177-85.

Abstract

BACKGROUND

Regulatory T cells (Tregs) have been involved in impaired immunity and may have a pivotal role in persistence of viral infections.

OBJECTIVE

To develop a simple and reliable in-house three color flow cytometery of peripheral blood to understand the role of HCV infection in the increase of Tregs.

METHODS

The level of naturally occurring CD4+ CD25+ FoxP3+ regulatory T cells (nTregs) in 20 chronically infected with hepatitis C virus (HCV) patients was compared to those of 15 healthy individuals by flowcytometry. In a different approach we performed permeabilization and intracellular staining before surface staining which allows the preservation of the surface molecules in the combined detection process and results in the normal frequency of nTregs in blood.

RESULTS

Using the optimized method, it was shown that a significantly higher proportion of nTregs in the total CD4+ T cell population was seen in the peripheral blood of chronic HCV patients (0.83 ± 0.21%, p=0.05) as compared to controls (0.26 ± 0.1, p=0.05).

CONCLUSIONS

In accordance with other studies, we showed that HCV infection induces a dramatic increase in Tregs, which might contribute to the immune response failure during HCV infection.

摘要

背景

调节性T细胞(Tregs)与免疫功能受损有关,可能在病毒感染的持续存在中起关键作用。

目的

开发一种简单可靠的外周血三色流式细胞术,以了解丙型肝炎病毒(HCV)感染在Tregs增加中的作用。

方法

通过流式细胞术比较20例慢性丙型肝炎病毒(HCV)感染患者与15例健康个体中自然产生的CD4+CD25+FoxP3+调节性T细胞(nTregs)的水平。在另一种方法中,我们在表面染色之前进行通透化和细胞内染色,这使得在联合检测过程中能够保留表面分子,并导致血液中nTregs的正常频率。

结果

使用优化的方法,结果显示,与对照组(0.26±0.1,p=0.05)相比,慢性HCV患者外周血中总CD4+T细胞群体中nTregs的比例显著更高(0.83±0.21%,p=0.05)。

结论

与其他研究一致,我们表明HCV感染会导致Tregs显著增加,这可能导致HCV感染期间免疫反应失败。

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