1624 Lymphocyte Products and the Macrophage Plasma Membrane

Infection of the mouse peritoneal cavity by bacillus Calmette-Gu6rin (BCG) 1 markedly alters the surface properties of macrophages (mob), compard with cells obtained from uninfected control animals or after injection of thioglycollate broth. BCG-activated peritoneal mob (BCG-PM) express enhanced Ia antigens (Ag), but reduced receptors for mannose-terminated glycoconjugates (MFR), Fc receptors, and m@speeific surface Ag F4/80 (1). Decreased receptor-mediated endocytosis is associated with active secretion of plasminogen activator (PA) (2), the ability to release 0 2 and H202 after surface stimulation (3, 4), and enhanced activity against various organisms and target cells (5, 6). The increase in Ia Ag (7-9) and in secretory (2, 10) and anti-microbial activity (11, 12) can depend on specifically sensitized T lymphocytes, and some of these effects are induced in nonactivated macrophages by treatment with lymphokines. Surface antigens and receptors control recognition and effector functions of activated m¢ and provide ideal markers to study the complex effects of lymphocyte products on macrophages. We show here that down-regulation of mannose-specific endocytosis and Ag F4/80 accompanies induction of mq~ Ia by Ag-stimulated T lymphocytes and lymphokines. These alterations in the plasma membrane make it possible to distinguish between activated and nonactivated macrophages and permit study of the mechanism of cell activation in vitro.