The Natural Killer Cell Response to HCV Infection
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understanding the role of natural killer (NK) cells in hepatitis C virus (HCV) infection. This includes multiple pathways by which HCV impairs or limits NK cells activation. Based on current genetic and functional data, a picture is emerging where only a rapid and strong NK cell response early on during infection which results in strong T cell responses and possible subsequent clearance, whereas chronic HCV infection is associated with dysfunctional or biased NK cells phenotypes. The hallmark of this NK cell dysfunction is persistent activation promoting ongoing hepatitis and hepatocyte damage, while being unable to clear HCV due to impaired IFN-γ responses. Furthermore, some data suggests certain chronically activated subsets that are NKp46high may be particularly active against hepatic stellate cells, a key player in hepatic fibrogenesis. Finally, the role of NK cells during HCV therapy, HCV recurrence after liver transplant and hepatocellular carcinoma are discussed.
Abstract
understanding the role of natural killer (NK) cells in hepatitis C virus (HCV) infection. This includes multiple pathways by which HCV impairs or limits NK cells activation. Based on current genetic and functional data, a picture is emerging where only a rapid and strong NK cell response early on during infection which results in strong T cell responses and possible subsequent clearance, whereas chronic HCV infection is associated with dysfunctional or biased NK cells phenotypes. The hallmark of this NK cell dysfunction is persistent activation promoting ongoing hepatitis and hepatocyte damage, while being unable to clear HCV due to impaired IFN-γ responses. Furthermore, some data suggests certain chronically activated subsets that are NKp46high may be particularly active against hepatic stellate cells, a key player in hepatic fibrogenesis. Finally, the role of NK cells during HCV therapy, HCV recurrence after liver transplant and hepatocellular carcinoma are discussed.
참고문헌 (80)
- "Fact Sheet No. 164"[URL]
- Hoofnagle, J. H., "Course and outcome of hepatitis C", Hepatology, 36, pp.S21~S29 (2002)
- Burra, P., "Hepatitis C. Semin", Liver Dis, 29, pp.53~65 (2009)
- NIH office of the director, "NIH consensus statement on management of hepatitis C", NIH Consens. State. Sci. Statements, 19, pp.1~46 (2002)
- Feld, J. J., "Mechanism of action of interferon and ribavirin in treatment of hepatitis C", Nature, 436, pp.967~972 (2005)
- Jacobson, I. M., "Telaprevir for previously untreated chronic hepatitis C virus infection", N. Engl. J. Med, 364, pp.2405~2416 (2011)
- Poordad, F., "Boceprevir for untreated chronic HCV genotype 1 infection", N. Engl. J. Med, 364, pp.1195~1206 (2011)
- Lee, S. H., "Keeping NK cells in highly regulated antiviral warfare", Trends Immunol, 28, pp.252~259 (2007)
- Moretta, L., "Human natural killer cells: their origin, receptors and function", Eur .J. Immunol, 32, pp.1205~1211 (2002)
- Hu, P. F., "Natural killer cell immunodeficiency in HIV disease is manifest by profoundly decreased numbers of CD16+CD56+ cells and expansion of a population of CD16dimCD56- cells with low lytic activity", J. Acquir Immune Defic. Syndr. Hum. Retrovirol, 10, pp.331~440 (1995)
- Mavilio, D., "Characterization of CD56-", CD16+ natural killer (NK) cells: a highly dysfunctional NK subset expanded in HIV-infected viremic individuals, 2005, pp.102, 2886~2891
- Ljunggren, H. G., "In search of the ‘missing self’: MHC molecules and NK cell recognition", Immunol Today, 11, pp.237~244 (1990)
- Cantoni, C., "NKp44, a triggering receptor involved in tumor cell lysis by activated human natural killer cells, is a novel member of the immunoglobulin superfamily", J. Exp. Med, 189, pp.787~796 (1999)
- Hata, K., "Isolation, phenotyping, and functional analysis of lymphocytes from human liver", Clin. Immunol. Immunopathol, 56, pp.401~419 (1990)
- Doherty, D. G., "nnate and adaptive lymphoid cells in the human liver", Immunol. Rev, 174, pp.5~20 (2000)
- Crotta, S., "Inhibition of natural killer cells through engagement of CD81 by the major hepatitis C virus envelope protein", J. Exp. Med, 195, pp.35~41 (2002)
- Tseng, C. T., "Binding of the hepatitis C virus envelope protein E2 to CD81 inhibits natural killer cell functions", J. Exp. Med, 195, pp.43~49 (2002)
- Crotta, S., "Hepatitis C virions subvert natural killer cell activation to generate a cytokine environment permissive for infection", J. Hepatol, 52, pp.183~190 (2010)
- Yoon, J. C., "Natural killer cell function is intact after direct exposure to infectious hepatitis C virions", Hepatology, 49, pp.12~21 (2009)
- Nattermann, J., "The HLA-A2 restricted T cell epitope HCV core 35-44 stabilizes HLA-E expression and inhibits cytolysis mediated by natural killer cells", Am. J. Pathol, 166, pp.443~453 (2005)
- Larkin, J., "Cytokine-activated natural killer cells exert direct killing of hepatoma cells harboring hepatitis C virus replicons", J. Interferon Cytokine Res, 26, pp.854~865 (2006)
- Yoon, J. C., "Cell-to-cell contact with hepatitis C virus-infected cells reduces functional capacity of natural killer cells", J. Virol, 85, pp.12557~12569 (2011)
- Wang, J. M., "KLRG1 negatively regulates natural killer (NK) cell functions through Akt pathway in individuals with chronic hepatitis C", J. Virol, 87, pp.11626~11636 (2013)
- Holder, K. A., "Hepatitis C Virus-Infected Cells Downregulate NKp30 and Inhibit Ex Vivo NK Cell Functions", J. Immunol, 191, pp.3308~3318 (2013)
- Nattermann, J., "Surface expression and cytolytic function of natural killer cell receptors is altered in chronic hepatitis C", Gut, 55, pp.869~877 (2006)
- Alter, G., "Reduced frequencies of NKp30+NKp46+, CD161+, and NKG2D+ NK cells in acute HCV infection may predict viral clearance", J. Hepatol, 55, pp.278~288 (2011)
- Golden-Mason, L., "Altered natural killer cell subset distributions in resolved and persistent hepatitis C virus infection following single source exposure", Gut, 57, pp.1121~1128 (2008)
- De Maria, A., "Increased natural cytotoxicity receptor expression and relevant IL-10 production in NK cells from chronically infected viremic HCV patients", Eur. J. Immunol, 37, pp.445~455 (2007)
- Oliviero, B., "Natural killer cell functional dichotomy in chronic hepatitis B and chronic hepatitis C virus infections", Gastroenterology, 137, pp.1151~1160 (2009)
- Stegmann, K. A., "Interferon alpha-stimulated natural killer cells from patients with acute hepatitis C virus (HCV) infection recognize HCV-infected and uninfected hepatoma cells via DNAX accessory molecule-1", J. Infect. Dis, 205, pp.1351~1362 (2012)
- Zhang, S., "IFN-gamma production by human natural killer cells in response to HCV-infected hepatoma cells is dependent on accessory cells", J. Hepatol, 59, pp.442~449 (2013)
- Sene, D., "Hepatitis C virus (HCV) evades NKG2D-dependent NK cell responses through NS5A-mediated imbalance of inflammatory cytokines", PLoS Pathog, 6, pp.e1001184~ (2010)
- Suppiah, V., "IL28B, HLA-C, and KIR variants additively predict response to therapy in chronic hepatitis C virus infection in a European Cohort: a cross-sectional study", PLoS Med, 8, pp.e1001092~ (2011)
- Knapp, S., "Consistent beneficial effects of killer cell immunoglobulin-like receptor 2DL3 and group 1 human leukocyte antigen-C following exposure to hepatitis C virus", Hepatology, 51, pp.1168~1175 (2010)
- Khakoo, S. I., "HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection", Science, 305, pp.872~874 (2004)
- Knapp, S., "A polymorphism in IL28B distinguishes exposed, uninfected individuals from spontaneous resolvers of HCV infection", Gastroenterology, 141, pp.320~325 (2011)
- Thomas, D. L., "Genetic variation in IL28B and spontaneous clearance of hepatitis C virus", Nature, 461, pp.798~801 (2009)
- Grebely, J., "Potential role for interleukin-28B genotype in treatment decision-making in recent hepatitis C virus infection", Hepatology, 52, pp.1216~1224 (2010)
- Suppiah, V., "IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy", Nat. Genet, 41, pp.1100~1104 (2009)
- Tanaka, Y., "Genome-wide association of IL28B with response to pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C", Nat. Genet, 41, pp.1105~1109 (2009)
- Ge, D., "Genetic variation in IL28B predicts hepatitis C treatment- induced viral clearance", Nature, 461, pp.399~401 (2009)
- Herzer, K., "Upregulation of major histocompatibility complex class I on liver cells by hepatitis C virus core protein via p53 and TAP1 impairs natural killer cell cytotoxicity", J. Virol, 77, pp.8299~8309 (2003)
- Ahlenstiel, G., "Distinct KIR", HLA compound genotypes affect the kinetics of human antiviral natural killer cell responses, 2008, pp.118, 1017~1026
- Shin, E. C., "Virus-induced type I IFN stimulates generation of immunoproteasomes at the site of infection", J. Clin. Invest, 116, pp.3006~3014 (2006)
- Thimme, R., "Viral and immunological determinants of hepatitis C virus clearance, persistence, and disease", Proc. Natl. Acad. Sci. USA, 99, pp.15661~15668 (2002)
- Guidotti, L. G., "To kill or to cure: options in host defense against viral infection", Curr. Opin. Immunol, 8, pp.478~483 (1996)
- Naggie, S., "Dysregulation of innate immunity in HCV genotype 1 IL28B unfavorable genotype patients: impaired viral kinetics and therapeutic response", Hepatology, 56, pp.444~454 (2012)
- Golden-Mason, L., "Natural killer inhibitory receptor expression associated with treatment failure and interleukin-28B genotype in patients with chronic hepatitis C", Hepatology, 54, pp.1559~1569 (2011)
- Amadei, B., "Activation of natural killer cells during acute infection with hepatitis C virus", Gastroenterology, 138, pp.1536~1545 (2010)
- Pelletier, S., "Increased degranulation of natural killer cells during acute HCV correlates with the magnitude of virus-specific T cell responses", J. Hepatol, 53, pp.805~816 (2010)
- Werner, J. M., "Innate immune responses in hepatitis C virus exposed healthcare workers who do not develop acute infection", Hepatology (2013)
- Ahlenstiel, G., "Natural killer cells are polarized toward cytotoxicity in chronic hepatitis C in an interferon- alfa-dependent manner", Gastroenterology, 138, pp.325~335 (2010)
- Edlich, B., "Early changes in interferon signaling define natural killer cell response and refractoriness to interferon- based therapy of hepatitis C patients", Hepatology, 55, pp.39~48 (2012)
- Miyagi, T., "High basal STAT4 balanced by STAT1 induction to control type 1 interferon effects in natural killer cells", J. Exp. Med, 204, pp.2383~2396 (2007)
- Miyagi, T., "Altered interferon-alpha-signaling in natural killer cells from patients with chronic hepatitis C virus infection", J. Hepatol, 53, pp.424~430 (2010)
- Varchetta, S., "Impaired intrahepatic natural killer cell cytotoxic function in chronic hepatitis C virus infection", Hepatology, 56, pp.841~849 (2012)
- Kramer, B., "Natural killer p46High expression defines a natural killer cell subset that is potentially involved in control of hepatitis C virus replication and modulation of liver fibrosis", Hepatology, 56, pp.1201~1213 (2012)
- Pembroke, T., "The paradox of NKp46+ natural killer cells: drivers of severe hepatitis C virus- induced pathology but in-vivo resistance to interferon alpha treatment", Gut (2013)
- Golden-Mason, L., "Race- and gender-related variation in natural killer p46 expression associated with differential anti- hepatitis C virus immunity", Hepatology, 56, pp.1214~1222 (2012)
- Eisenhardt, M., "The CXCR3(+)CD56Bright phenotype characterizes a distinct NK cell subset with anti-fibrotic potential that shows dys-regulated activity in hepatitis C", PLoS. One, 7, pp.e38846~ (2012)
- Biron, C. A., "Natural killer cells in antiviral defense: function and regulation by innate cytokines", Annu. Rev. Immunol, 17, pp.189~220 (1999)
- Kaser, A., "Interferon-alpha (IFN-alpha) enhances cytotoxicity in healthy volunteers and chronic hepatitis C infection mainly by the perforin pathway", Clin. Exp. Immunol, 118, pp.71~77 (1999)
- Bozzano, F., "Activating NK cell receptor expression", function (NKp30, NKp46, DNAM-1) during chronic viraemic HCV infection is associated with the outcome of combined treatment, 2011, pp.41, 2905~2914
- Conry, S. J., "Genetically associated CD16(+)56(-) natural killer cell interferon (IFN)-αR expression regulates signaling and is implicated in IFN-α-induced hepatitis C virus decline", J. Infect. Dis, 205, pp.1131~1141 (2012)
- Ahlenstiel, G., "Early changes in natural killer cell function indicate virologic response to interferon therapy for hepatitis C", Gastroenterology, 141, pp.1231~1239 (2011)
- Lagging, M., "IP-10 predicts viral response and therapeutic outcome in difficult- to-treat patients with HCV genotype 1 infection", Hepatology, 44, pp.1617~1625 (2006)
- Oliviero, B., "Natural killer cell dynamic profile is associated with treatment outcome in patients with chronic HCV infection", J. Hepatol, 59, pp.38~44 (2013)
- Dring, M. M., "Innate immune genes synergize to predict increased risk of chronic disease in hepatitis C virus infection", Proc. Natl. Acad. Sci. USA, 108, pp.5736~5741 (2011)
- Kramer, B., "Do lambda- IFNs IL28A and IL28B act on human natural killer cells?", Proc. Natl. Acad. Sci. USA, 108, pp.E519~E520 (2011)
- O’Connor, K. S., "IFNL3 mediates interaction between innate immune cells: Implications for hepatitis C virus pathogenesis", Innate. Immun (2013)
- Stegmann, K. A., "Interferon alpha induces TRAIL on natural killer cells is associated with control of hepatitis C virus infection", Gastroenterology, 138, pp.1885~1897 (2010)
- Gane, E. J., "Long-term outcome of hepatitis C infection after liver transplantation", N. Engl. J. Med, 334, pp.815~820 (1996)
- Feray, C., "European collaborative study on factors influencing outcome after liver transplantation for hepatitis C. European Concerted Action on Viral Hepatitis (EUROHEP) Group", Gastroenterology, 117, pp.619~625 (1999)
- de Arias, A. E., "Killer cell immunoglobulin-like receptor genotype and killer cell immunoglobulin-like receptor-human leukocyte antigen C ligand compatibility affect the severity of hepatitis C virus recurrence after liver transplantation", Liver Transpl, 15, pp.390~399 (2009)
- Legaz, I., "KIR gene mismatching and KIR", C ligands in liver transplantation: consequences for short-term liver allograft injury, 2013, pp.95, 1037~1044
- Moya-Quiles, M. R., "Impact of recipient HLA-C in liver transplant: a protective effect of HLA-Cw*07 on acute rejection", Hum. Immunol, 68, pp.51~58 (2007)
- Varchetta, S., "Prospective study of natural killer cell phenotype in recurrent hepatitis C virus infection following liver transplantation", J. Hepatol, 50, pp.314~322 (2009)
- Trinchieri, G., "Biology of natural killer cells", Adv. Immunol, 47, pp.187~376 (1989)
- Lopez-Vazquez, A., "Protective effect of the HLA-Bw4I80 epitope and the killer cell immunoglobulin- like receptor 3DS1 gene against the development of hepatocellular carcinoma in patients with hepatitis C virus infection", J. Infect. Dis, 192, pp.162~165 (2005)
- Yuen, M. F., "Expression of inhibitory receptors in natural killer (CD3(-)CD56(+)) cells and CD3(+)CD56(+) cells in the peripheral blood lymphocytes and tumor infiltrating lymphocytes in patients with primary hepatocellular carcinoma", Clin. Immunol, 101, pp.264~269 (2001)
