丙型肝炎病毒与先天性和适应性免疫反应：共同进化与共存的故事
Hepatitis C virus versus innate and adaptive immune responses: a tale of coevolution and coexistence.
作者信息
Rehermann Barbara
机构信息
Immunology Section, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH/DHHS, Bethesda, MD 20892, USA.
出版信息
J Clin Invest. 2009 Jul;119(7):1745-54. doi: 10.1172/JCI39133. Epub 2009 Jul 1.
Abstract
Since the identification of the hepatitis C virus (HCV) 20 years ago, much progress has been made in our understanding of its life cycle and interaction with the host immune system. Much has been learned from HCV itself, which, via decades of coevolution, gained an intricate knowledge of host innate and adaptive immune responses and developed sophisticated ways to preempt, subvert, and antagonize them. This review discusses the clinical, virological, and immunological features of acute and chronic hepatitis C and the role of the immune response in spontaneous and treatment-induced HCV clearance.
摘要
自20年前丙型肝炎病毒（HCV）被发现以来，我们对其生命周期以及与宿主免疫系统相互作用的理解取得了很大进展。从HCV自身我们了解到很多情况，经过数十年的共同进化，它对宿主的固有免疫和适应性免疫反应有了深入认识，并形成了先发制人、颠覆和对抗这些反应的复杂方式。本文综述了急性和慢性丙型肝炎的临床、病毒学和免疫学特征，以及免疫反应在自发清除和治疗诱导清除HCV中的作用。
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Synergistic reversal of intrahepatic HCV-specific CD8 T cell exhaustion by combined PD-1/CTLA-4 blockade.通过联合阻断PD-1/CTLA-4协同逆转肝内丙型肝炎病毒特异性CD8 T细胞耗竭
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PD-L1 negatively regulates CD4+CD25+Foxp3+ Tregs by limiting STAT-5 phosphorylation in patients chronically infected with HCV.在慢性丙型肝炎病毒感染患者中，程序性死亡受体配体1（PD-L1）通过限制信号转导子和转录激活子5（STAT-5）磷酸化对CD4+CD25+叉头框蛋白3+调节性T细胞（Tregs）产生负向调节作用。
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