参考文献 References
[1] Hedley-Whyte J, Milamed DR. Hepatitis B: Prevalence, Hope [J]. Ulster Med J, 2019, 88(2):118-123.
[2] Jiang Y, Han Q, Zhao H, et al. The Mechanisms of HBV-Induced HepatocellularCarcinoma [J]. J Hepatocell Carcinoma, 2021, 8: 35-450.
[3] Sun C, Sun H, Zhang C, et al. NK cell receptor imbalance and NK cell dysfunction in HBVinfection and hepatocellular carcinoma [J]. Cell Mol Immunol, 2015, 12(3): 292-302.
[4] Yuan L, Jiang J, Liu X, et al. HBV infection-induced liver cirrhosis development indual-humanised mice with human bone mesenchymal stem cell transplantation [J]. Gut, 2019,68(11): 2044-2056.
[5] 赵斐, 刘菲, 王中峰, 等. HBV垂直传播形式及阻断策略 [J]. 临床肝胆病杂志,2019,35(11):2557-2559.
[6] Tsai KN, Kuo CF, Ou JJ. Mechanisms of Hepatitis B Virus Persistence [J]. Trends Microbiol, 2018, 26(1): 33-42.
[7] Chisari FV, Isogawa M, Wieland SF. Pathogenesis of hepatitis B virus infection [J]. Pathol Biol(Paris), 2010, 58(4): 258-66.
[8] Kulik L, El-Serag HB. Epidemiology and Management of Hepatocellular Carcinoma [J].Gastroenterology, 2019, 156(2): 477-491.
[9] Li H, Yan L, Shi Y, et al. Hepatitis B Virus Infection: Overview [J]. Adv Exp Med Biol. 2020,1179: 1-16.
[10] Spyrou E, Smith CI, Ghany MG. Hepatitis B: Current Status of Therapy and Future Therapies [J]. Gastroenterol Clin North Am, 2020, 49(2): 215-238.
[11] Spearman CW. Towards the elimination of hepatitis B and hepatocellular carcinoma [J]. S AfrMed J, 2018, 108(8b): 13-16.
[12] Yoon EL. Prophylactic Antiviral Treatment in Immunosuppressed Chronic Hepatitis BPatients [J]. Korean J Gastroenterol, 2019, 74(5): 258-266.
[13] Stojanovic A, Cerwenka A. ILC1-like NK cells as matchmakers for DC-T cell interactions [J].Immunity, 2021, 54(10): 2185-2187.
[14] Sun C, Sun H, Zhang C, et al. NK cell receptor imbalance and NK cell dysfunction in HBVinfection and hepatocellular carcinoma [J]. Cell Mol Immunol, 2015, 12(3): 292-302.
[15] Yu WH, Cosgrove C, Berger CT, et al. ADCC-Mediated CD56DIM NK Cell Responses AreAssociated with Early HBsAg Clearance in Acute HBV Infection [J]. Pathog Immun, 2018,3(1): 2-18.
[16] El-Darawish Y, Li W, Yamanishi K, et al. Frontline Science: IL-18 primes murine NK cells forproliferation by promoting protein synthesis, survival, and autophagy [J]. J Leukoc Biol, 2018,104(2): 253-264.
[17] Ziblat A, Domaica CI, Spallanzani RG, et al. IL-27 stimulates human NK-cell effectorfunctions and primes NK cells for IL-18 responsiveness [J]. Eur J Immunol, 2015, 45(1):192-202.
[18] Fisicaro P, Rossi M, Vecchi A, et al. The Good and the Bad of Natural Killer Cells in VirusControl: Perspective for Anti-HBV Therapy [J]. Int J Mol Sci, 2019, 20(20): 5080.
[19] Li F, Wei H, Wei H, et al. Blocking the natural killer cell inhibitory receptor NKG2Aincreases activity of human natural killer cells and clears hepatitis B virus infection in mice [J]. Gastroenterology, 2013,144(2): 392-401.
[20] Braud VM, Allan DS, O'Callaghan CA, et al. HLA-E binds to natural killer cell receptorsCD94/NKG2A, B and C [J]. Nature, 1998, 391(6669): 795-9.
[21] Yoshioka T, Tatsumi T, Miyagi T, et al. Frequency and role of NKp46 and NKG2A in hepatitisB virus infection [J]. PLoS One, 2017, 12(3): e0174103.
[22] Meresse B, Chen Z, Ciszewski C, et al. Coordinated induction by IL15 of a TCR-independentNKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiacdisease [J]. Immunity, 2004, 21(3): 357-66.
[23] Chen T, Zhu L, Shi A, et al. Functional restoration of CD56bright NK cells facilitates immunecontrol via IL-15 and NKG2D in patients under antiviral treatment for chronic hepatitis B [J].Hepatol Int, 2017, 11(5): 419-428.
[24] Shen X, Fu B, Liu Y, et al. NKp30+ NK cells are associated with HBV control duringpegylated-interferon-alpha-2b therapy of chronic hepatitis B [J]. Sci Rep, 2016, 6: 38778.
[25] Zhang C, Zhang J, Sun R, et al. Opposing effect of IFNgamma and IFNalpha on expression ofNKG2 receptors: negative regulation of IFNgamma on NK cells [J]. Int Immunopharmacol,2005, 5(6): 1057-67.
[26] Tjwa ET, van Oord GW, Hegmans JP, et al. Viral load reduction improves activation andfunction of natural killer cells in patients with chronic hepatitis B [J]. J Hepatol, 2011, 54(2):209-18.
[27] Boltjes A, van Montfoort N, Biesta PJ, et al. Kupffer cells interact with hepatitis B surfaceantigen in vivo and in vitro, leading to proinflammatory cytokine production and natural killercell function [J]. J Infect Dis, 2015, 211(8): 1268-78.
[28] Tripp CS, Wolf SF, Unanue ER. Interleukin 12 and tumor necrosis factor alpha arecostimulators of interferon gamma production by natural killer cells in severe combinedimmunodeficiency mice with listeriosis, and interleukin 10 is a physiologic antagonist [J]. ProcNatl Acad Sci USA, 1993, 90(8): 3725-9.
[29] Li H, Zhai N, Wang Z, et al. Regulatory NK cells mediated between immunosuppressivemonocytes and dysfunctional T cells in chronic HBV infection [J]. Gut, 2018, 67(11):2035-2044.
[30] Dolina JS, Sung SS, Novobrantseva TI, et al. Lipidoid Nanoparticles Containing PD-L1siRNA Delivered In Vivo Enter Kupffer Cells and Enhance NK and CD8(+) T Cell-mediatedHepatic Antiviral Immunity [J]. Mol Ther Nucleic Acids, 2013, 2(2): e72.
[31] Zannetti C, Roblot G, Charrier E, et al. Characterization of the Inflammasome in HumanKupffer Cells in Response to Synthetic Agonists and Pathogens [J]. J Immunol, 2016, 197(1):356-67.
[32] Lopes AR, Kellam P, Das A, et al. Bim-mediated deletion of antigen-specific CD8 T cells inpatients unable to control HBV infection [J]. J Clin Invest, 2008, 118(5): 1835-45.
[33] Peppa D, Gill US, Reynolds G, et al. Up-regulation of a death receptor renders antiviral Tcells susceptible to NK cell-mediated deletion [J]. J Exp Med, 2013, 210(1): 99-114.
[34] Fröhlich A, Kisielow J, Schmitz I, et al. IL-21R on T cells is critical for sustainedfunctionality and control of chronic viral infection [J]. Science, 2009, 324(5934): 1576-80.
[35] Waggoner SN, Daniels KA, Welsh RM. Therapeutic depletion of natural killer cells controlspersistent infection [J]. J Virol, 2014, 88(4): 1953-60.
[36] Chen Y, Sun R, Wu X, et al. CD4+CD25+ Regulatory T Cells Inhibit Natural Killer Cell Hepatocytotoxicity of Hepatitis B Virus Transgenic Mice via Membrane-Bound TGF-β andOX40 [J]. J Innate Immun, 2016, 8(1): 30-42.
[37] Cooper MA, Fehniger TA, Fuchs A, et al. NK cell and DC interactions [J]. Trends Immunol,2004, 25(1): 47-52.
[38] Wehner R, Dietze K, Bachmann M, et al. The bidirectional crosstalk between human dendriticcells and natural killer cells [J]. J Innate Immun, 2011, 3(3): 258-63.
[39] Shi CC, Tjwa ET, Biesta PJ, et al. Hepatitis B virus suppresses the functional interactionbetween natural killer cells and plasmacytoid dendritic cells [J]. J Viral Hepat, 2012, 19(2):e26-33.
[40] Golsaz-Shirazi F, Amiri MM, Shokri F. Immune function of plasmacytoid dendritic cells,natural killer cells, and their crosstalk in HBV infection [J]. Rev Med Virol, 2018, 28(6): e2007.
[41] Woltman AM, Op den Brouw ML, Biesta PJ, et al. Hepatitis B virus lacks immune activatingcapacity, but actively inhibits plasmacytoid dendritic cell function [J]. PLoS One, 2011, 6(1):e15324.
[42] 42. Okazaki A, Hiraga N, Imamura M, et al. Severe necroinflammatory reaction caused by natural killer cell-mediated Fas/Fas ligand interaction and dendritic cells in human hepatocyte chimericmouse [J]. Hepatology, 2012, 56(2): 555-66.
[43] Gao B, Radaeva S. Natural killer and natural killer T cells in liver fibrosis [J]. Biochimica etbiophysica acta, 2013, 1832(7): 1061-9.
[44] Muhanna N, Abutair L, Doron S, et al. Amelioration of hepatic fibrosis by NK cell activation[J]. Gut, 2011, 60(1): 90-8.
[45] Melhem A, Muhanna N, Bishara, et al. Anti-fibrotic activity of NK cells in experimental liverinjury through killing of activated HSC [J]. Journal of Hepatology, 2006, 45(1): 60-71.
[46] Jeong WI, Park O, Gao B. Abrogation of the antifibrotic effects of natural killercells/interferon-gamma contributes to alcohol acceleration of liver fibrosis [J].Gastroenterology, 2008, 134(1): 248-58.
[47] Jeong WI, Park O, Radaeva S, et al. STAT1 inhibits liver fibrosis in mice by inhibiting stellatecell proliferation and stimulating NK cell cytotoxicity [J]. Hepatology, 2006, 44(6): 1441-51.
[48] Weng H, Mertens PR, Gressner AM, et al. IFN-gamma abrogates profibrogenic TGF-betasignaling in liver by targeting expression of inhibitory and receptor Smads [J]. Journal ofHepatology, 2007, 46(2): 295-303.
[49] Li T, Yang Y, Song H, et al. Activated NK cells kill hepatic stellate cells via p38/PI3Ksignaling in a TRAIL-involved degranulation manner [J]. J Leukoc Biol, 2019, 105(4):695-704.
[50] Jiang Y, Yang M, Sun X, et al. IL-10+ NK and TGF-β+ NK cells play negative regulatoryroles in HIV infection [J]. BMC Infect Dis, 2018, 18(1): 80.
[51] Ostapchuk YO, Cetin EA, Perfilyeva YV, et al. Peripheral blood NK cells expressing HLA-G,IL-10 and TGF-beta in healthy donors and breast cancer patients [J]. Cell Immunol, 2015, 298(1-2): 37-46.
[52] Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013 [J]. CA Cancer J Clin, 2013, 63(1):11-30.
[53] Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015 [J]. CA Cancer J Clin,2016, 66(2): 115-32.
[54] Zhao LH, Liu X, Yan HX, et al. Genomic and oncogenic preference of HBV integration inhepatocellular carcinoma [J]. Nat Commun, 2016, 7: 12992.
[55] Lim CJ, Lee YH, Pan L, et al. Multidimensional analyses reveal distinct immunemicroenvironment in hepatitis B virus-related hepatocellular carcinoma [J]. Gut, 2019, 68:916-927.
[56] Curran CS, Sharon E. PD-1 immunobiology in autoimmune hepatitis and hepatocellularcarcinoma [J]. Semin Oncol, 2017, 44: 428-432.
[57] Kamiya T, Chang YH, Campana D. Expanded and Activated Natural Killer Cells forImmunotherapy of Hepatocellular Carcinoma [J]. Cancer Immunol Res, 2016, 4: 574-581.
[58] Liu Y, Cheng Y, Xu Y, et al. Increased expression of programmed cell death protein 1 on NKcells inhibits NK-cell-mediated anti-tumor function and indicates poor prognosis in digestivecancers [J]. Oncogene, 2017, 36: 6143-6153.