Differential Tumor Surveillance by Natural Killer (Nk) and Nkt Cells

DOI PDF 被引用文献23件
  • Mark J. Smyth
    aFrom the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
  • Kevin Y. T. Thia
    aFrom the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
  • Shayna E.A. Street
    aFrom the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
  • Erika Cretney
    aFrom the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
  • Joseph A. Trapani
    aFrom the Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia
  • Masaru Taniguchi
    bDivision of Molecular Immunology, Center of Biomedical Sciences, School of Medicine, Chiba University, Chiba 260-8670, Japan
  • Tetsu Kawano
    bDivision of Molecular Immunology, Center of Biomedical Sciences, School of Medicine, Chiba University, Chiba 260-8670, Japan
  • Sonja B. Pelikan
    cDepartment of Pathology and Immunology, Monash University Medical School, Prahran, 3181 Victoria, Australia
  • Nadine Y. Crowe
    cDepartment of Pathology and Immunology, Monash University Medical School, Prahran, 3181 Victoria, Australia
  • Dale I. Godfrey
    cDepartment of Pathology and Immunology, Monash University Medical School, Prahran, 3181 Victoria, Australia

抄録

<jats:p>Natural tumor surveillance capabilities of the host were investigated in six different mouse tumor models where endogenous interleukin (IL)-12 does or does not dictate the efficiency of the innate immune response. Gene-targeted and lymphocyte subset–depleted mice were used to establish the relative importance of natural killer (NK) and NK1.1+ T (NKT) cells in protection from tumor initiation and metastasis. In the models examined, CD3− NK cells were responsible for tumor rejection and protection from metastasis in models where control of major histocompatibility complex class I–deficient tumors was independent of IL-12. A protective role for NKT cells was only observed when tumor rejection required endogenous IL-12 activity. In particular, T cell receptor Jα281 gene-targeted mice confirmed a critical function for NKT cells in protection from spontaneous tumors initiated by the chemical carcinogen, methylcholanthrene. This is the first description of an antitumor function for NKT cells in the absence of exogenously administered potent stimulators such as IL-12 or α-galactosylceramide.</jats:p>

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