Cytotoxic activity of interferon-treated macrophages studied by various inhibitors.
The ability of interferon-treated macrophages to kill or inhibit the growth of tumor cells is markedly influenced by the local environment. The macrophage cytotoxic effector system is regulated by serum and other environmental factors that suppress tumor killing. Prostaglandins E1 and E2, but not F2alpha reversibly inhibited the tumoricidal state of interferon-treated macrophages. Hydrocortisone was similarly active at suppressing macrophage function. Such nonimmunologically derived factors could prevent the final triggering step for macrophage-mediated tumor killing in the local environment of the tumor and may be important in the pathogenesis of progressive tumor growth.
D000818:Animals; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D006854:Hydrocortisone / Q000494:pharmacology*; D007372:Interferons / Q000494:pharmacology*; D007942:Leukemia, Experimental / Q000628:therapy; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051379:Mice; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*
D011459:Prostaglandins E, Synthetic; D007372:Interferons; D006854:Hydrocortisone