The present study seeks to reassess the roles of macrophage activation and persistent firm binding to tumor cells as a prerequisite for tumoricidal activity. To this end, macrophage effector populations from various tissues, expressing diverse functional activities, were made to interact in vitro with different suspension tumor cell lines. The resultant binding and cytolytic effector cell capacities were determined. Macrophage activation appears to be an absolute prerequisite for binding and for killing of tumor cells. Activated macrophages firmly bind and form clusters with D-12 rat fibrosarcoma cells, which are relatively resistant to macrophage-mediated tumoricidal action. In contrast, P-815 murine mastocytoma cells, highly susceptible to the lytic activity of macrophages, bind rather poorly with activated macrophages and do not form clusters. Since susceptible target cells are readily killed by activated rat macrophages in the absence of persistent firm contact, it appears that firm binding and killing are not causally related events.
No takes yet. Share an insight, caveat, or question.
Keller et al. (1986) studied this question.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: