Prevention of interferon-induced augmentation of cellular antitumor effector mechanisms by phorbol esters.
Both natural killer cell- and macrophage-mediated spontaneous in vitro cytotoxicity for tumor targets is rapidly and strongly augmented by interferon. Macrophage-activating lymphokines considerably enhance macrophage-tumoricidal activity but did not affect natural killer cell-type cytotoxicity. Augmentation of cytolytic capacity by interferon and by macrophage-activating lymphokines is prevented by the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate. However, the classical antiviral activity and the specific binding of interferon to cell surface receptors remains unaffected by 12-O-tetradecanoylphorbol-13-acetate.
D000818:Animals; D007372:Interferons / Q000037:antagonists & inhibitors* / Q000378:metabolism; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D009369:Neoplasms / Q000276:immunology*; D010704:Phorbols / Q000633:toxicity*; D013755:Tetradecanoylphorbol Acetate / Q000633:toxicity*; D014779:Virus Replication / Q000187:drug effects
D010704:Phorbols; D007372:Interferons; D013755:Tetradecanoylphorbol Acetate