Abstract
Treatment with a unique lymphokine enables resident mouse peritoneal macrophages to phagocytize via their complement (C) receptors; the lymphokine acts by enabling C receptor engagement by C3b ligands to generate a phagocytic signal, thereby linking the cell surface binding event with the intracellular phagocytic machinery. Immobilized immune complexes were used to study the topography of C3b receptors of resident mouse peritoneal macrophages treated with the lymphokine. Lymphokine treatment apparently enables the macrophages'' C3b receptors to migrate within the plane of the cells'' plasma membrane; manipulations of macrophages that abrogate 1 response to lymphokine, C rceptor mobility, also abrogate the other response, C receptor-mediated phagocytosis. Lateral mobility of a ligand-bound receptor within the macrophage plasma membrane probably is an essential component of the phagocytic signal. The difference in C receptor function among various populations of macrophages apparently is not due to the expression of different types of C receptors by the different macrophage populations but rather to a difference in the relationship of the C3b receptor with other plasma membrane or intracellular components.