Hepatitis C Virus-Mediated Modulation of Cellular Immunity
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REVIEW
Hepatitis C Virus-Mediated Modulation of Cellular Immunity Erwin Daniel Brenndo¨rfer • Matti Sa¨llberg
Received: 20 October 2011 / Accepted: 9 March 2012 / Published online: 22 August 2012 Ó L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2012
Abstract The hepatitis C virus (HCV) is a major cause of chronic liver disease globally. A chronic infection can result in liver fibrosis, liver cirrhosis, hepatocellular carcinoma and liver failure in a significant ratio of the patients. About 170 million people are currently infected with HCV. Since 80 % of the infected patients develop a chronic infection, HCV has evolved sophisticated escape strategies to evade both the innate and the adaptive immune system. Thus, chronic hepatitis C is characterized by perturbations in the number, subset composition and/or functionality of natural killer cells, natural killer T cells, dendritic cells, macrophages and T cells. The balance between HCV-induced immune evasion and the antiviral immune response results in chronic liver inflammation and consequent immune-mediated liver injury. This review summarizes our current understanding of the HCV-mediated interference with cellular immunity and of the factors resulting in HCV persistence. A profound knowledge about the intrinsic properties of HCV and its effects on intrahepatic immunity is essential to be able to design effective immunotherapies against HCV such as therapeutic HCV vaccines.
Abbreviations DAA Directly acting antiviral DC Dendritic cell HCV Hepatitis C virus HLA Human leukocyte antigen IFN Interferon IL Interleukin KIR Killer cell immunoglobulin-like receptor MHC Major histocompatibility complex NK cell Natural killer cell NKT cell Natural killer T cell NS Non-structural PBMC Peripheral blood mononuclear cell PD Programmed death TCR T cell receptor TGF Tumor growth factor Th T-helper cell TIM T cell immunoglobulin domain and mucin domain protein TLR Toll-like receptor TNF Tumor necrosis factor Treg Regulatory T cell
Keywords HCV Kupffer cells Dendritic cells NK cells NKT cells Adaptive immune response Introduction
E. D. Brenndo¨rfer (&) M. Sa¨llberg Division of Clinical Microbiology F68, Department of Laboratory Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden e-mail: [email protected] M. Sa¨llberg e-mail: [email protected]
With approximately 170 million people infected with hepatitis C virus (HCV) globally, HCV represents a significant health burden. An infection with HCV is characterized by a probability of 70–80 % to develop a chronic infection accompanied by liver inflammation which causes liver fibrosis, cirrhosis and an increased risk to develop hepatocellular carcinoma in 30 % of the cases (Lauer and Walker 2001; Liang et al. 2000; Poynard et al.
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2003). Since the current treatment based on pegylated interferon (IFN)-a and ribavirin can cure only about 55 % of the treated patients and is associated with various side effects, more efficient th
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