RECEPTOR FUNCTION IN VITRO I. Characterization of the Cellular Interactions Required for the Generation of a T-Lymphocyte Product that Enhances Macrophage Complement Receptor Function*

The plasma membranes of phagocytic leukocytes have receptors for the Fc portion of IgG (1-6) and for a cleavage product of the third component of complement, C3 (3, 4, 6-8). These receptors are distinct from one another (1-3) and serve different functions in promoting the interaction of phagocytic cells with immunologically coated particles and soluble material in the cells' environment (6-10). Several investigators have demonstrated that the C3b receptors of mouse peritoneal macrophages (6-9) and other phagocytic cells (11) mediate binding, but not ingestion, of C3b-coated particles. Bianco et al. (8) have previously found that the C3b receptors of mouse peritoneal macrophages elicited by the i.p. injection of thioglycollate medium mediate both binding and ingestion of C3b-coated particles. It was not possible in those studies to determine whether thioglycollate medium altered macrophage complement receptor function by inducing the influx of a physiologically different population of mononuclear phagocytes into the peritoneal cavity, by altering the number or density of complement receptors of resident peritoneal macrophages, or by inducing a qualitative change in the function of complement receptors of the resident macrophage population. To understand better the cellular and molecular mechanisms by which such changes in complement receptor function may occur in vivo, we undertook to determine the in vitro conditions under which the function of macrophage complement receptors could be modified. Because available evidence suggests that thioglycollate-elicited macrophages behave similarly in many respects to macrophages that have been influenced by lymphokines (12-15), our initial efforts were directed at examining the effects of antigen-stimulted lymphocytes and their products upon macrophage complement receptor function. However, in experiments in which lymphocytes and macrophages from bacille Calmette Gu~rin-infected mice were cultivated together in the presence of appropriate antigen, we were unable to detect any