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本文引用的文献

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Parallel expansion of human virus-specific FoxP3- effector memory and de novo-generated FoxP3+ regulatory CD8+ T cells upon antigen recognition in vitro.体外抗原识别后,人类病毒特异性FoxP3效应记忆细胞和新生FoxP3 +调节性CD8 + T细胞的平行扩增。
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Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression.调节性T细胞上表达的CD39和CD73催化生成的腺苷介导免疫抑制。
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Cyclic adenosine monophosphate is a key component of regulatory T cell-mediated suppression.环磷酸腺苷是调节性T细胞介导的免疫抑制的关键组成部分。
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Quantification and localisation of FOXP3+ T lymphocytes and relation to hepatic inflammation during chronic HCV infection.慢性丙型肝炎病毒感染期间FOXP3 + T淋巴细胞的定量、定位及其与肝脏炎症的关系。
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FOXP3 modifies the phenotypic and functional properties of regulatory T cells.FOXP3可改变调节性T细胞的表型和功能特性。
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Hepatitis C virus (HCV)-specific CD8+ cells produce transforming growth factor beta that can suppress HCV-specific T-cell responses.丙型肝炎病毒(HCV)特异性CD8 +细胞产生可抑制HCV特异性T细胞反应的转化生长因子β。
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Cutting Edge: IL-2 is essential for TGF-beta-mediated induction of Foxp3+ T regulatory cells.前沿:白细胞介素-2对于转化生长因子-β介导的叉头框蛋白3阳性调节性T细胞的诱导至关重要。
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The dynamic co-evolution of memory and regulatory CD4+ T cells in the periphery.外周记忆性与调节性CD4+ T细胞的动态协同进化
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Foxp3 occupancy and regulation of key target genes during T-cell stimulation.T细胞刺激过程中Foxp3对关键靶基因的占据及调控
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病毒性肝炎中的调节性T细胞。

Regulatory T cells in viral hepatitis.

作者信息

Billerbeck Eva, Bottler Tobias, Thimme Robert

机构信息

Department of Medicine II, University Hospital Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany.

出版信息

World J Gastroenterol. 2007 Sep 28;13(36):4858-64. doi: 10.3748/wjg.v13.i36.4858.

DOI:10.3748/wjg.v13.i36.4858
PMID:17828817
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4611764/
Abstract

The pathogenesis and outcome of viral infections are significantly influenced by the host immune response. The immune system is able to eliminate many viruses in the acute phase of infection. However, some viruses, like hepatitis C virus (HCV) and hepatitis B virus (HBV), can evade the host immune responses and establish a persistent infection. HCV and HBV persistence is caused by various mechanisms, like subversion of innate immune responses by viral factors, the emergence of T cell escape mutations, or T cell dysfunction and suppression. Recently, it has become evident that regulatory T cells may contribute to the pathogenesis and outcome of viral infections by suppressing antiviral immune responses. Indeed, the control of HCV and HBV specific immune responses mediated by regulatory T cells may be one mechanism that favors viral persistence, but it may also prevent the host from overwhelming T cell activity and liver damage. This review will focus on the role of regulatory T cells in viral hepatitis.

摘要

病毒感染的发病机制和转归受到宿主免疫反应的显著影响。免疫系统能够在感染急性期清除许多病毒。然而,一些病毒,如丙型肝炎病毒(HCV)和乙型肝炎病毒(HBV),能够逃避宿主免疫反应并建立持续感染。HCV和HBV的持续感染是由多种机制引起的,如病毒因子对固有免疫反应的破坏、T细胞逃逸突变的出现,或T细胞功能障碍及抑制。最近,有证据表明调节性T细胞可能通过抑制抗病毒免疫反应而在病毒感染的发病机制和转归中发挥作用。事实上,调节性T细胞介导的对HCV和HBV特异性免疫反应的控制可能是有利于病毒持续感染的一种机制,但它也可能防止宿主出现过度的T细胞活性和肝损伤。本综述将聚焦于调节性T细胞在病毒性肝炎中的作用。