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慢性丙型肝炎病毒感染中单核细胞和T细胞中Toll样受体的不同表达

Distinct Toll-like receptor expression in monocytes and T cells in chronic HCV infection.

作者信息

Dolganiuc Angela, Garcia Catherine, Kodys Karen, Szabo Gyongyi

机构信息

University of Massachusetts Medical School, Department of Medicine, 364 Plantation Street, Worcester, MA 01605-2324, United States.

出版信息

World J Gastroenterol. 2006 Feb 28;12(8):1198-204. doi: 10.3748/wjg.v12.i8.1198.

Abstract

AIM

Hepatitis C virus often establishes chronic infections. Recent studies suggest that viral and bacterial infections are more common in HCV-infected patients compared to controls. Pathogens are recognized by Toll-like receptors (TLRs) to shape adaptive and innate immune responses.

METHODS

In this study, to assess the ability of HCV-infected host to recognize invading pathogens, we investigated Toll-like receptor expression in innate (monocytes) and adaptive (T cells) immune cells by real-time PCR.

RESULTS

We determined that RNA levels for TLRs 2, 6. 7, 8, 9 and 10 mRNA levels were upregulated in both monocytes and T cells in HCV-infected patients compared to controls. TLR4 was only upregulated in T lymphocytes, while TLR5 was selectively increased in monocytes of HCV-infected patients. MD-2, a TLR4 co-receptor, was increased in patients' monocytes and T cells while CD14 and MyD88 were increased only in monocytes.

CONCLUSION

Our data reveal novel details on TLR expression that likely relates to innate recognition of pathogens and immune defense in HCV-infected individuals.

摘要

目的

丙型肝炎病毒常引发慢性感染。近期研究表明,与对照组相比,丙型肝炎病毒感染患者中病毒和细菌感染更为常见。病原体通过Toll样受体(TLR)被识别,从而形成适应性和先天性免疫反应。

方法

在本研究中,为评估丙型肝炎病毒感染宿主识别入侵病原体的能力,我们通过实时PCR研究了先天性免疫细胞(单核细胞)和适应性免疫细胞(T细胞)中Toll样受体的表达。

结果

我们确定,与对照组相比,丙型肝炎病毒感染患者的单核细胞和T细胞中TLR2、6、7、8、9和10的mRNA水平均上调。TLR4仅在T淋巴细胞中上调,而TLR5在丙型肝炎病毒感染患者的单核细胞中选择性增加。TLR4共受体MD-2在患者的单核细胞和T细胞中增加,而CD14和MyD88仅在单核细胞中增加。

结论

我们的数据揭示了TLR表达的新细节,这可能与丙型肝炎病毒感染个体中病原体的先天性识别和免疫防御有关。

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本文引用的文献

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Management of Hepatitis C in HIV-infected Patients.HIV感染患者的丙型肝炎管理
Curr Infect Dis Rep. 2005 Mar;7(2):91-102. doi: 10.1007/s11908-005-0067-0.

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