Preexposure of resting B cells to interferon-gamma enhances their proliferative response to subsequent activation signals.
In this report we demonstrate that pretreatment of resting splenic B cells with IFN-gamma increases their mitogenic response to subsequent activating stimuli. This effect is completely blocked by neutralizing anti-IFN-gamma antibodies. By contrast, a similar effect induced by partially purified BCGF is not completely inhibited by anti-IFN-gamma antibody, inferring that as in the mouse, a B-cell-specific factor may also induce increased responsiveness to mitogens in resting B cells. The mechanism of this response was analyzed. Phenotypic and cell cycle analyses of the IFN-gamma-treated cells following activation were not significantly different from control cells with respect to kinetics, although as expected from thymidine uptake, more cells were actively cycling. Even when a very early manifestation of cell activation, Ca2+ flux was examined, no response to IFN-gamma alone was evoked, and the response to subsequent activation was identical to that of control cells. These data show that IFN-gamma did not directly activate B cells, but primed B cells in a manner which amplified subsequent mitogenesis.
D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000954:Antigens, Surface / Q000032:analysis; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D002453:Cell Cycle / Q000187:drug effects; D002478:Cells, Cultured; D006133:Growth Substances / Q000494:pharmacology; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D066298:In Vitro Techniques; D007371:Interferon-gamma / Q000494:pharmacology*; D015847:Interleukin-4; D008213:Lymphocyte Activation / Q000187:drug effects*; D008222:Lymphokines / Q000494:pharmacology
D000888:Antibodies, Anti-Idiotypic; D000954:Antigens, Surface; D006133:Growth Substances; D008222:Lymphokines; D015847:Interleukin-4; D007371:Interferon-gamma