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INTERACTION OF INTERFERON, MACROPHAGE AND LYMPHOCYTE TUMORICIDAL ACTIVITY WITH PROSTAGLANDIN EFFECT

The vital role of mononuclear phagocytes in host defense against neoplasia, as well as infectious organisms, has been amply demonstrated. Little, however, is known concerning the ability of specific agents which are capable of modifying the functional activity of macrophages. There appears to be a close relationship between the ability of biological and synthetic agents to enhance host antitumor resistance and their capacity to activate macrophages. Increasing evidence suggests that the activated macrophage is a major effector of tumor surveillance, rather than the specifically immunologically active lymphocyte. It then becomes important to better understand the mechanisms by which these agents are involved in the pharmacological control of the macrophage system. By judiciously controlling macrophage activity to express a tumoricidal or tumor-stasis effect, through agents capable of enhancing this effect, it is possible to combine a tumor cytoreductive therapy with a macrophage-activating agent, thus enhancing tumor reduction. Recent results indicate that fibroblast interferon or several interferon inducers have the capacity to activate macrophages to exert a tumoricidal activity. This report will present the current findings of our laboratory studies devoted to defining the mechanisms through which macrophages exert a tumoricidal effect and factors affecting this response.