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Open AccessOpen Access JUSTC Original Paper

Innate recognition and immune regulation of NK

  • Institute of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei 230027, China

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  • Corresponding author: TIAN Zhi-gang, E-mail: tzg@ustc.edu.cn
  • Received Date: 20 June 2008
  • Rev Recd Date: 02 July 2008
  • Publish Date: 31 August 2008
    Abstract

  • Abstract

    Natural killer receptors (NKRs) and Toll-like receptors (TLRs) are the most important receptor supfamilies in innate immunity and act as first line of host defense against infection or transformed cells. These receptors exert peculiar recognition mechanisms to sense danger signals and distinguish infectious nonself from noninfectious self, and thereafter work as link molecules between innate and adaptive immunity. NK cells are the most important lymphocytes population, recognize infection and tumor at initial, and play a critical role in linking innate immunity with adaptive immunity. In this paper, we highlight the importance of recognition and interaction of those receptors via NK cells. The precise mechanisms can be harnessed to aid the rational design of therapy against infection, inflammation, cancer or autoimmune diseases.

    Abstract

    Natural killer receptors (NKRs) and Toll-like receptors (TLRs) are the most important receptor supfamilies in innate immunity and act as first line of host defense against infection or transformed cells. These receptors exert peculiar recognition mechanisms to sense danger signals and distinguish infectious nonself from noninfectious self, and thereafter work as link molecules between innate and adaptive immunity. NK cells are the most important lymphocytes population, recognize infection and tumor at initial, and play a critical role in linking innate immunity with adaptive immunity. In this paper, we highlight the importance of recognition and interaction of those receptors via NK cells. The precise mechanisms can be harnessed to aid the rational design of therapy against infection, inflammation, cancer or autoimmune diseases.
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    • References(66)
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    [1]
    Trinchieri G, Sher A. Cooperation of Toll-like receptor signals in innate immune defence[J]. Nat Rev Immunol, 2007,7(3):179-190.
    [2]
    Miyake K. Innate immune sensing of pathogens and danger signals by cell surface Toll-like receptors[J]. Semin Immunol, 2007,19 (1):3-10.
    [3]
    Kawai T, Akira S. TLR signaling[J]. Semin Immunol, 2007,19(1):24-32.
    [4]
    Moretta L, Bottino C, Pende D, et al. Surface NK receptors and their ligands on tumor cells[J]. Semin Immunol, 2006,18(3):151-158.
    [5]
    Kabelitz D, Medzhitov R. Innate immunity: Cross-talk with adaptive immunity through pattern recognition receptors and cytokines[J]. Curr Opin Immunol, 2007, 19(1):1-3.
    [6]
    Moretta L, Moretta A. Unravelling natural killer cell function: Triggering and inhibitory human NK receptors[J]. EMBO J, 2004,23(2): 255-259.
    [7]
    Zhang C, Zhang J, Wei H, et al. Imbalance of NKG2D and its inhibitory counterparts: How does tumor escape from innate immunity[J]. Int Immunopharmacol, 2005, 5(7-8):1 099-1 111.
    [8]
    Wu P, Wei H, Zhang C, et al. Regulation of NK cell activation by stimulatory and inhibitory receptors in tumor escape from innate immunity[J]. Front Biosci, 2005,10:3 132-3 142.
    [9]
    Ljunggren H G, Krre K. In search of the “missing self”: MHC molecules and NK cell recognition[J]. Immunol Today, 1990,11(7):237-244.
    [10]
    Raulet D H. Roles of the NKG2D immunoreceptor and its ligands[J]. Nat Rev Immunol, 2003,3(10):781-790.
    [11]
    Watzl C. The NKG2D receptor and its ligands-recognition beyond the “missing self”[J]. Microbes and Infection, 2003,5(1):31-37.
    [12]
    魏海明，邬鹏，田志刚. NK细胞识别的新模式：压力诱导模式[J]. 中国肿瘤生物治疗杂志，2005,12(2):85-88.
    [13]
    Long E O, Rajagopalan S. Stress signals activate natural killer cells[J]. J Exp Med, 2002,196(11):1 399-1 402.
    [14]
    Michalsson J, Teixeira de Matos C, Achour A, et al. A signal peptide derived from hsp60 binds HLA-E and interferes with CD94/NKG2A recognition[J]. J Exp Med, 2002,196(11):1 403-1 414.
    [15]
    Hamerman J A, Ogasawara K, Lanier L L. Cutting edge: Toll-like receptor signaling in macrophages induces ligands for the NKG2D receptor[J]. J Immunol, 2004,172(4): 2 001-2 005.
    [16]
    Schreiner B, Voss J, Wischhusen J, et al. Expression of toll-like receptors by human muscle cells in vitro and in vivo: TLR3 is highly expressed in inflammatory and HIV myopathies, mediates IL-8 release and up-regulation of NKG2D-ligands[J]. FASEB J, 2006,20(1):118-120.
    [17]
    Dong Z, Wei H, Sun R, et al. Involvement of natural killer cells in PolyI:C-induced liver injury[J]. J Hepatol, 2004,41(6):966-973.
    [18]
    Wang J, Sun R, Wei H, et al. Pre-activation of T lymphocytes by low dose of concanavalin A aggravates toll-like receptor-3 ligand-induced NK cell-mediated liver injury[J]. Int Immunopharmacol, 2006,6(5):800-807.
    [19]
    Wang J, Sun R, Wei H, et al. Poly I:C prevents T cell-mediated hepatitis via an NK-dependent mechanism[J]. J Hepatol, 2006,44(3):446-454.
    [20]
    Jiang W, Sun R, Wei H, Tian Z. Toll-like receptor 3 ligand attenuates LPS-induced liver injury by down-regulation of toll-like receptor 4 expression on macrophages[J]. Proc Natl Acad Sci U S A, 2005,102(47):17 077-17 082.
    [21]
    Radaeva S, Sun R, Jaruga B, et al. Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners[J]. Gastroenterology, 2006,130(2):435-452.
    [22]
    Chen Y, Sun R, Jiang W, et al. Liver-specific HBsAg transgenic mice are over-sensitive to Poly（I:C）-induced liver injury in NK cell-and IFN-gamma-dependent manner[J]. J Hepatol, 2007,47(2):183-190.
    [23]
    Zhang J, Sun R, Wei H, et al. Toll-like receptor 3 agonist enhances IFN-gamma and TNF-alpha production by murine uterine NK cells[J]. Int Immunopharmacol, 2007,7(5):588-596.
    [24]
    Zhang J, Wei H, Wu D, Tian Z. Toll-like receptor 3 agonist induces impairment of uterine vascular remodeling and fetal losses in CBAxDBA/2 mice[J]. J Reprod Immunol, 2007,74(1-2):61-67.
    [25]
    Zhou R, Wei H, Sun R, et al. NKG2D recognition mediates Toll-like receptor 3 signaling-induced breakdown of epithelial homeostasis in the small intestines of mice[J]. Proc Natl Acad Sci U S A, 2007,104(18):7 512-7 515.
    [26]
    Zhou R, Wei H, Sun R, Tian Z. Recognition of double-stranded RNA by TLR3 induces severe small intestinal injury in mice[J]. J Immunol, 2007,178(7):4 548-4 556.
    [27]
    Zhou R, Wei H, Tian Z. NK3-like NK cells are involved in protective effect of polyinosinic-polycytidylic acid on type 1 diabetes in nonobese diabetic mice[J]. J Immunol, 2007,178(4):2 141-2 147.
    [28]
    Hart OM, Athie-Morales V, OConnor G M, et al. TLR7/8-mediated activation of human NK cells results in accessory cell-dependent IFN-γ production[J]. J Immunol, 2005,175(3):1 636-1 642.
    [29]
    Sawaki J, Tsutsui H, Hayashi N, et al. Type 1 cytokine/chemokine production by mouse NK cells following activation of their TLR/MyD88-mediated pathways[J]. Int Immunol, 2007,19(3):311-320.
    [30]
    Newman K C, Riley E M. Whatever turns you on: Accessory-cell-dependent activation of NK cells by pathogens[J]. Nat Rev Immunol, 2007, 7(4):279-291.
    [31]
    Cooper M A, Fehniger T A, Fuchs A, et al. NK cell and DC interactions[J]. Trends Immunol, 2004, 25(1):47-52.
    [32]
    Moretta A. Natural killer cells and dendritic cells: Rendezvous in abused tissues[J]. Nat Rev Immunol, 2002,2:957-963.
    [33]
    Raulet D. Interplay of natural killer cells and their receptors with the adaptive immune responses[J]. Nat Immunol, 2004, 5(10): 996-1 002.
    [34]
    Zitvogel L. Dendritic and Natural killer cells cooperate in the control/switch of innate immunity[J]. J Exp Med, 2002,195(3):F9-F14.
    [35]
    Moretta L, Ferlazzo G, Mingari M C, et al. Human natural killer cell function and their interactions with dendritic cells[J]. Vaccine, 2003,21 Suppl 2:S38-42.
    [36]
    Geldhof A B, Van Ginderachter J A, Liu Y, et al. Antagonistic effect of NK cells on alternatively activated monocytes: a contribution of NK cells to CTL generation[J]. Blood, 2002, 100: 4 049-4 058.
    [37]
    Kelly J M, Darcy P K, Markby J L, et al. Induction of tumor-specific T cell memory by NK cell-mediated tumor rejection[J]. Nat Immunol, 2002, 3(1):83-90.
    [38]
    Wilcox R A, Tamada K, Strome S E, et al. Signaling through NK cell-associated CD137 promotes both helper function for CD8+ cytolytic T cells and responsiveness to IL-2 but not cytolytic activity[J]. J Immunol, 2002,169(8):4 230-4 236.
    [39]
    Assarsson E, Kambayashi T, Schatzle J D, et al. NK cells stimulate proliferation of T and NK cells through 2B4/CD48 interactions[J]. J Immunol, 2004,173:174-180.
    [40]
    Zingoni A, Sornasse T, Cocks B G, et al. NK cell regulation of T cell-mediated responses[J]. Mol Immunol, 2005, 42:451-454.
    [41]
    Hanna J, Gonen-Gross T, Fitchett J, et al. Novel APC-like properties of human NK cells directly regulate T cell activation[J]. J Clin Invest, 2004, 114:1 612-1 623.
    [42]
    Zhang R, Zheng X, Li B, et al. Human NK cells positively regulate gammadelta T cells in response to Mycobacterium tuberculosis[J]. J Immunol, 2006, 176(4):2 610-2 616.
    [43]
    Della Chiesa M, Vitale M, Carlomagno S, et al. The natural killer cell-mediated killing of autologous dendritic cells is confined to a cell subset expressing CD94/NKG2A, but lacking inhibitory killer Ig-like receptors[J]. Eur J Immunol, 2003, 33: 1 657-1 666.
    [44]
    Trivedi P P, Roberts P C, Wolf N A, et al. NK cells inhibit T cell proliferation via p21-mediated cell cycle arrest[J]. J Immunol, 2005,174(8):4 590-4 597.
    [45]
    Takeda K, Hayakawa Y, Van Kaer L, et al. Critical contribution of liver natural killer T cells to a murine model of hepatitis[J]. Proc Natl Acad Sci U S A, 2000, 97(10):5 498-5 503.
    [46]
    Chen Y, Wei H, Sun R, et al. Increased susceptibility to liver injury in hepatitis B virus transgenic mice involves NKG2D-ligand interaction and natural killer cells[J]. Hepatology, 2007,46(3):706-715.
    [47]
    Dong Z, Zhang J, Sun R, et al. Impairment of liver regeneration correlates with activated hepatic NKT cells in HBV transgenic mice[J]. Hepatology, 2007, 45(6):1 400-1 412.
    [48]
    Li B, Sun R, Wei H, et al. Interleukin-15 prevents concanavalin A-induced liver injury in mice via NKT cell-dependent mechanism[J]. Hepatology, 2006, 43(6):1 211-1 219.
    [49]
    Chen Q, Wei H, Sun R, et al. Therapeutic RNA silencing of Cys-X3-Cys chemokine ligand 1 gene prevents mice from adenovirus vector-induced acute liver injury[J]. Hepatology, 2008, 47(2):648-658.
    [50]
    Gao B, Jeong W I, Tian Z. Liver: An organ with predominant innate immunity[J]. Hepatology, 2008, 47(2):729-736.
    [51]
    Dong Z, Wei H, Sun R, Tian Z. The roles of innate immune cells in liver injury and regeneration[J]. Cell Mol Immunol, 2007, 4(4):241-252.
    [52]
    Xu W, Fazekas G, Hara H, et al. Mechanism of natural killer (NK) cell regulatory role in experimental autoimmune encephalomyelitis[J]. J Neuroimmunol, 2005,163(1-2):24-30.
    [53]
    Takahashi K, Aranami T, Endoh M, et al. The regulatory role of natural killer cells in multiple sclerosis[J]. Brain, 2004,127(Pt 9):1 917-1 927.
    [54]
    Cooper M A, Fehniger T A, Caligiuri M A, et al. The biology of human natural killer-cell subsets[J]. Trends Immunol, 2001, 22: 633-640.
    [55]
    Jacobs R, Hintzen G, Kemper A, et al. CD56bright cells differ in their KIR repertoire and cytotoxic features from CD56dim NK cells[J]. Eur J Immunol, 2001, 31: 3 121-3 126.
    [56]
    Zheng X, Wang Y, Wei H, et al. Bcl-xL is associated with the anti-apoptotic effect of IL-15 on the survival of CD56dim natural killer cells[J]. Mol Immunol 2008(in press).
    [57]
    Bauernhofer T, Kuss I, Henderson B, et al. Preferential apoptosis of CD56dim natural killer cell subset in patients with cancer[J]. Eur J Immunol, 2003, 33:119-124.
    [58]
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