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Gastroenterology
Volume 138, Issue 1
, Pages 325-335.e2
, January 2010
Natural Killer Cells Are Polarized Toward Cytotoxicity in Chronic Hepatitis C in an Interferon-Alfa–Dependent Manner
References
- . Immunology of hepatitis B virus and hepatitis C virus infection. Nat Rev Immunol. 2005;5:215–229
- Heterologous T cell immunity in severe hepatitis C virus infection. J Exp Med. 2005;201:675–680
- Analysis of successful immune responses in persons infected with hepatitis C virus. J Exp Med. 2000;191:1499–1512
- Differential CD4 and CD8 T-cell responsiveness in hepatitis C virus infection. Hepatology. 2001;33:267–276
- High resolution analysis of cellular immune responses in resolved and persistent hepatitis C virus infection. Gastroenterology. 2004;127:924–936
- Impaired effector function of hepatitis C virus-specific CD8+ T cells in chronic hepatitis C virus infection. J Immunol. 2002;169:3447–3458
- Liver-infiltrating lymphocytes in chronic human hepatitis C virus infection display an exhausted phenotype with high levels of PD-1 and low levels of CD127 expression. J Virol. 2007;81:2545–2553
- High-programmed death-1 levels on hepatitis C virus-specific T cells during acute infection are associated with viral persistence and require preservation of cognate antigen during chronic infection. J Immunol. 2008;181:8215–8225
- Resident human hepatic lymphocytes are phenotypically different from circulating lymphocytes. J Hepatol. 1998;28:84–90
- . Accumulation of natural killer and cytotoxic T large granular lymphocytes in the liver during virus infection. J Exp Med. 1986;164:1667–1681
- Cytokines induced during chronic hepatitis B virus infection promote a pathway for NK cell-mediated liver damage. J Exp Med. 2007;204:667–680
- HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection. Science. 2004;305:872–874
- Increased frequencies of activating natural killer receptors are associated with liver injury in individuals who do not eliminate hepatitis C virus. Tissue Antigens. 2007;69(Suppl 1):109–111
- Distinct KIR/HLA compound genotypes affect the kinetics of human antiviral natural killer cell responses. J Clin Invest. 2008;118:1017–1026
- Cytokine-activated NK cells exert direct killing of hepatoma cells harboring hepatitis C virus replicons. J Interferon Cytokine Res. 2006;26:854–865
- Altered natural killer cell subset distributions in resolved and persistent hepatitis C virus infection following single source exposure. Gut. 2008;57:1121–1128
- Decreased NK cell frequency in chronic hepatitis C does not affect ex vivo cytolytic killing. Hepatology. 2006;43:573–580
- Surface expression and cytolytic function of natural killer cell receptors is altered in chronic hepatitis C. Gut. 2006;55:869–877
- Increased natural cytotoxicity receptor expression and relevant IL-10 production in NK cells from chronically infected viremic HCV patients. Eur J Immunol. 2007;37:445–455
- Natural killer cell functional dichotomy in chronic hepatitis B and chronic hepatitis C virus infections. Gastroenterology. 2009;137:1151–1160
- . Binding of the hepatitis C virus envelope protein E2 to CD81 inhibits natural killer cell functions. J Exp Med. 2002;195:43–49
- Inhibition of natural killer cells through engagement of CD81 by the major hepatitis C Virus envelope protein. J Exp Med. 2002;195:35–42
- Natural killer cell function is intact after direct exposure to infectious hepatitis C virions. Hepatology. 2009;49:12–21
- . CD107a as a functional marker for the identification of natural killer cell activity. J Immunol Methods. 2004;294:15–22
- Differential cytokine and chemokine gene expression by human NK cells following activation with IL-18 or IL-15 in combination with IL-12: implications for the innate immune response. J Immunol. 1999;162:4511–4520
- IL-12-dependent inducible expression of the CD94/NKG2A inhibitory receptor regulates CD94/NKG2C+ NK cell function. J Immunol. 2009;182:829–836
- Human natural killer cells: their origin, receptors and function. Eur J Immunol. 2002;32:1205–1211
- Natural killer cells in antiviral defence: function and regulation by innate cytokines. Annu Rev Immunol. 1999;17:189–220
- High basal STAT4 balanced by STAT1 induction to control type 1 interferon effects in natural killer cells. J Exp Med. 2007;204:2383–2396
- Shared alterations in NK cell frequency, phenotype, and function in chronic human immunodeficiency virus and hepatitis C virus infections. J Virol. 2005;79:12365–12374
- Genomic analysis of the host response to hepatitis C virus infection. Proc Natl Acad Sci U S A. 2002;99:15669–15674
- . DNA microarray analysis of chimpanzee liver during acute resolving hepatitis C virus infection. J Virol. 2001;75:7059–7066
- Virus-induced type I IFN stimulates generation of immunoproteasomes at the site of infection. J Clin Invest. 2006;116:3006–3014
- Enhanced expression of interferon-regulated genes in the liver of patients with chronic hepatitis C virus infection: detection by suppression-subtractive hybridization. J Virol. 2001;75:1332–1338
- IFNalpha regulates NK cell cytotoxicity through STAT1 pathway. Cytokine. 2003;23:190–199
- Tumour necrosis factor related apoptosis inducing ligand (TRAIL) induces hepatic steatosis in viral hepatitis and after alcohol intake. Gut. 2005;54:1590–1596
- Hepatitis C virus infection sensitizes human hepatocytes to TRAIL-induced apoptosis in a caspase 9-dependent manner. J Immunol. 2008;181:4926–4935
- Hepatitis C virus triggers apoptosis of a newly developed hepatoma cell line through antiviral defense system. Gastroenterology. 2007;133:1649–1659
- Natural killer cells suppress full cycle HCV infection of human hepatocytes. J Viral Hepat. 2008;15:855–864
- Viral and immunological determinants of hepatitis C virus clearance, persistence, and disease. Proc Natl Acad Sci U S A. 2002;99:15661–15668
- . To kill or to cure: options in host defense against viral infection. Curr Opin Immunol. 1996;8:478–483
- NK cells of human secondary lymphoid tissues enhance T cell polarization via IFN-gamma secretion. Eur J Immunol. 2006;36:2394–2400
- Hepatic gene expression during treatment with peginterferon and ribavirin: identifying molecular pathways for treatment response. Hepatology. 2007;46:1548–1563
Conflicts of interest The authors disclose no conflicts.
Funding This study was supported by the intramural research program of the National Institute for Diabetes and Digestive and Kidney Diseases, National Institutes of Health; and Golo Ahlenstiel is the recipient of grant AH173/1-1 from the Deutsche Forschungsgemein-Schaft, Bonn, Germany.
PII: S0016-5085(09)01559-5
doi: 10.1053/j.gastro.2009.08.066
© 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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Gastroenterology
Volume 138, Issue 1
, Pages 325-335.e2
, January 2010

