|
1）Garcia-Sastre A, Biron CA. Type 1 interferons and the virus-host relationship: a lesson in detente . Science. 2006; 312: 879-82
|
|
|
|
2）Lee SH, Miyagi T, Biron CA. Keeping NK cells in highly regulated antiviral warfare. Trends Immunol. 2007; 28: 252-9
|
|
|
|
|
3）Kelly C, Klenerman P, Barnes E. Interferon lambdas: the next cytokine storm. Gut. 2011; 60: 1284-93
|
|
|
|
|
|
4）Rehermann B. Hepatitis C virus versus innate and adaptive immune responses: a tale of coevolution and coexistence. J Clin Invest. 2009; 119: 1745-54
|
|
|
|
|
|
5）Thomas E, Gonzalez VD, Li Q, et al. HCV infection induces a unique hepatic innate immune response associated with robust production of type III interferons. Gastro-enterology. 2012; 142: 978-88
|
|
|
|
|
|
6）Park H, Serti E, Eke O, et al. IL-29 is the dominant type III interferon produced by hepatocytes during acute hepatitis C virus infection. Hepatology. In press
|
|
|
|
|
|
7）Marukian S, Andrus L, Sheahan TP, et al. Hepatitis C virus induces interferon-λ and interferon-stimulated genes in primary liver cultures. Hepatology. 2011; 54: 1913-23
|
|
|
|
|
|
8）Thomas DL, Thio CL, Martin MP, et al. Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature. 2009; 461: 798-801
|
|
|
|
|
|
9）Khakoo SI, Thio CL, Martin MP, et al. HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection. Science. 2004; 305: 872-4
|
|
|
|
|
|
10）Alter G, Jost S, Rihn S, et al. Reduced frequencies of NKp30+NKp46+, CD161+, and NKG2D+ NK cells in acute HCV infection may predict viral clearance. J Hepatol. 2011; 55: 278-88
|
|
|
|
|
|
11）Amadei B, Urbani S, Cazaly A, et al. Activation of natural killer cells during acute infection with hepatitis C virus. Gastroenterology. 2010; 138: 1536-45
|
|
|
|
|
|
12）Pelletier S, Drouin C, Bedard N, et al. Increased degranulation of natural killer cells during acute HCV correlates with the magnitude of virus-specific T cell responses. J Hepatol. 2010; 53: 805-16
|
|
|
|
|
|
13）Dring MM, Morrison MH, McSharry BP, et al. Innate immune genes synergize to predict increased risk of chronic disease in hepatitis C virus infection. Proc Natl Acad Sci U S A. 2011; 108: 5736-41
|
|
|
|
|
|
14）Ahlenstiel G, Titerence RH, Koh C, et al. Natural killer cells are polarized toward cytotoxicity in chronic hepatitis C in an interferon-alfa-dependent manner. Gastroenterology. 2010; 138: 325-35
|
|
|
|
|
|
15）Miyagi T, Takehara T, Nishio K, et al. Altered interferon-alpha-signaling in natural killer cells from patients with chronic hepatitis C virus infection. J Hepatol. 2010; 53: 424-30
|
|
|
|
|
|
16）Golden-Mason L, Stone AE, Bambha KM, et al. Race- and gender-related variation in NKp46 expression associated with differential anti-HCV immunity. Hepatology. In press
|
|
|
|
|
|
17）Krämer B, Korner C, Kebschull M, et al. NKp46(High) expression defines a NK cell subset that is potentially involved in control of HCV replication and modulation of liver fibrosis. Hepatology. In press
|
|
|
|
|
|
18）McMahan RH, Golden-Mason L, Nishimura MI, et al. Tim-3 expression on PD-1+ HCV-specific human CTLs is associated with viral persistence, and its blockade restores hepatocyte-directed in vitro cytotoxicity. J Clin Invest. 2010; 120: 4546-57
|
|
|
|
|
|
19）Raziorrouh B, Ulsenheimer A, Schraut W, et al. Inhibitory molecules that regulate expansion and restoration of HCV-specific CD4+ T cells in patients with chronic infection. Gastroenterology. 2011; 141: 1422-31
|
|
|
|
|
|
20）Ge D, Fellay J, Thompson AJ, et al. Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance. Nature. 2009; 461: 399-401
|
|
|
|
|
|
21）Suppiah V, Moldovan M, Ahlenstiel G, et al. IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy. Nat Genet. 2009; 41: 1100-4
|
|
|
|
|
|
22）Tanaka Y, Nishida N, Sugiyama M, et al. Genome-wide association of IL28B with response to pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C. Nat Genet. 2009; 41: 1105-9
|
|
|
|
|
|
23）Honda M, Sakai A, Yamashita T, et al. Hepatic ISG expression is associated with genetic variation in interleukin 28B and the outcome of IFN therapy for chronic hepatitis C. Gastro-enterology. 2010; 139: 499-509
|
|
|
|
|
|
24）OBrien TR. Interferon-alfa, interferon-lambda and hepatitis C. Nat Genet. 2009; 41: 1048-50
|
|
|
|
|
|
25）Suppiah V, Gaudieri S, Armstrong NJ, et al. 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. 2011; 8: e1001092
|
|
|
|
|
|
26）Ahlenstiel G, Edlich B, Hogdal LJ, et al. Early changes in natural killer cell function indicate virologic response to interferon therapy for hepatitis C. Gastroenterology. 2011; 141: 1231-9
|
|
|
|
|
|
27）Edlich B, Ahlenstiel G, Azpiroz AZ, et al. Early changes in interferon signaling define natural killer cell response and refractoriness to interferon-based therapy of hepatitis C patients. Hepatology. 2012; 55: 39-48
|
|
|
|
|
|
28）Golden-Mason L, Bambha KM, Cheng L, et al. Natural killer inhibitory receptor expression associated with treatment failure and interleukin-28B genotype in patients with chronic hepatitis C. Hepatology. 2011; 54: 1559-69
|
|
|
|
|
|
29）Zhang Z, Zhang S, Zou Z, et al. Hypercytolytic activity of hepatic natural killer cells correlates with liver injury in chronic hepatitis B patients. Hepatology. 2011; 53: 73-85
|
|
|
|
|
|
30）Tjwa ET, van Oord GW, Hegmans JP, et al. Viral load reduction improves activation and function of natural killer cells in patients with chronic hepatitis B. J Hepatol. 2011; 54: 209-18
|
|
|
|
|
|
31）Kumar V, Kato N, Urabe Y, et al. Genome-wide association study identifies a susceptibility locus for HCV-induced hepatocellular carcinoma. Nat Genet. 2011; 43: 455-8
|
|
|
|
|
|
32）Hoshida Y, Fuchs BC, Tanabe KK. Genomic risk of hepatitis C-related hepatocellular carcinoma. J Hepatol. 2012; 56: 729-30
|
|
|
|
|
|
33）Jinushi M, Takehara T, Tatsumi T, et al. Expression and role of MICA and MICB in human hepatocellular carcinomas and their regulation by retinoic acid. Int J Cancer. 2003; 104: 354-61
|
|
|
|
|
|
34）Jinushi M, Takehara T, Tatsumi T, et al. Impairment of natural killer cell and dendritic cell functions by the soluble form of MHC class I-related chain A in advanced human hepatocellular carcinomas. J Hepatol. 2005; 43: 1013-20
|
|
|
|
|
|
35）Kohga K, Takehara T, Tatsumi T, et al. Serum levels of soluble major histocompatibility complex (MHC) class I-related chain A in patients with chronic liver diseases and changes during transcatheter arterial embolization for hepato-cellular carcinoma. Cancer Sci. 2008; 99: 1643-9
|
|
|
|
|
36）Chew V, Tow C, Teo M, et al. Inflammatory tumour microenvironment is associated with superior survival in hepatocellular carcinoma patients. J Hepatol. 2010; 52: 370-9
|
|
|
|
|
|
37）Chew V, Chen J, Lee D, et al. Chemokine-driven lymphocyte infiltration: an early intratumoural event determining long-term survival in resect-able hepatocellular carcinoma. Gut. 2012; 61: 427-38
|
|
|
|
|