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      Involvement of tumor necrosis factor-related apoptosis-inducing ligand in NK cell-mediated and IFN-gamma-dependent suppression of subcutaneous tumor growth.

      Cellular Immunology
      Animals, Antibodies, Monoclonal, immunology, pharmacology, Apoptosis Regulatory Proteins, Carcinoma, Renal Cell, pathology, Cytotoxicity, Immunologic, Fibrosarcoma, Immunity, Innate, Immunologic Surveillance, Injections, Subcutaneous, Interferon-gamma, deficiency, genetics, physiology, Kidney Neoplasms, Killer Cells, Natural, L Cells (Cell Line), transplantation, Male, Mast-Cell Sarcoma, Melanoma, Experimental, Membrane Glycoproteins, antagonists & inhibitors, Mice, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Knockout, Mice, SCID, Neoplasm Transplantation, Neoplasms, Experimental, Perforin, Pore Forming Cytotoxic Proteins, TNF-Related Apoptosis-Inducing Ligand, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha

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          Abstract

          Natural killer (NK) cells and interferon- (IFN) gamma have been implicated in immune surveillance against tumor development. Here we show tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is a type II membrane protein belonging to the TNF family and plays a critical role in the NK cell-mediated and IFN-gamma-dependent suppression of subcutaneous growth of TRAIL-sensitive tumors. Administration of a neutralizing monoclonal antibody against TRAIL promoted outgrowth of subcutaneously inoculated TRAIL-sensitive tumors (L929, LB27.4, and Renca) but not TRAIL-resistant tumors (P815 and B16). Such a protective effect of TRAIL against TRAIL-sensitive tumors was abrogated in NK cell-depleted or IFN-gamma-deficient mice. These results suggested a substantial role of TRAIL as the effector molecule that eliminates subcutaneously developing TRAIL-sensitive tumors.

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