Activation and proliferation signals in mouse B cells. II. Evidence for activation (G0 to G1) signals differing in sensitivity to cyclosporine.
We have previously shown that cyclosporine (CS) selectively inhibits polyclonal activation of B cells by anti-Ig antibodies but not by lipopolysaccharide (LPS). Here we extend these results using a two-stage B cell culture system in which cells from either CBA/N or normal mice are activated to enter G1 by anti-Ig, and are then stimulated to proliferate by LPS. In this system CS blocks an event that occurs within 4 h after initial activation, i.e. prevents entry of B cells into G1. Phorbol myristic acetate also induces some CBA/N B cells to enter G1. However, activation of B cells by this agent is resistant to inhibition by CS. These data suggest that there are two biochemically distinct mechanisms for driving resting B cells into G1. A hypothesis to explain these results is presented.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000502:physiology; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D003524:Cyclosporins / Q000494:pharmacology*; D005260:Female; D007399:Interphase / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000888:Antibodies, Anti-Idiotypic; D003524:Cyclosporins; D008070:Lipopolysaccharides; D013755:Tetradecanoylphorbol Acetate