NIHR Biomedical Research Centre, Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.
Gut. 2012 Aug;61(8):1226-34. doi: 10.1136/gutjnl-2011-300620. Epub 2011 Aug 28.
Over recent years, it has become increasingly accepted that virus-specific CD4+ and CD8+ T cell responses play a major role in outcome and pathogenesis of hepatitis C virus (HCV) infection. Indeed, while the emergence of strong and multispecific T cell responses may correlate with spontaneous viral clearance, the virus has developed several mechanisms to avoid T cell control in the majority of acutely HCV-infected patients that subsequently develop persistent HCV infection. In this review, we will discuss the current knowledge about the role of cellular immune responses in HCV infection. Specifically, we will emphasise recent new insights into the effector functions of T cells, possible mechanisms of their failure and the host-virus interactions occurring at the site of the disease, the liver.
近年来，人们越来越接受这样一种观点，即病毒特异性 CD4+和 CD8+T 细胞应答在丙型肝炎病毒（HCV）感染的结局和发病机制中起着重要作用。事实上，虽然强烈的多特异性 T 细胞应答的出现可能与自发性病毒清除相关，但病毒已经发展出几种机制来逃避大多数急性 HCV 感染患者的 T 细胞控制，这些患者随后会发展为持续性 HCV 感染。在这篇综述中，我们将讨论细胞免疫应答在 HCV 感染中的作用的现有知识。具体而言，我们将强调 T 细胞效应功能的最新见解、它们失效的可能机制以及发生在疾病部位（肝脏）的宿主-病毒相互作用。
