Preexposure of resting B cells to interferon-γ enhances their proliferative response to subsequent activation signals

In this report we demonstrate that pretreatment of resting splenic B cells with IFN-γ increases their mitogenic response to subsequent activating stimuli. This effect is completely blocked by neutralizing anti-IFN-γ antibodies. By contrast, a similar effect induced by partially purified BCGF is not completely inhibited by anti-IFN-γ 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-γ-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, Ca 2+ flux was examined, no response to IFN-γ alone was evoked, and the response to subsequent activation was identical to that of control cells. These data show that IFN-γ did not directly activate B cells, but primed B cells in a manner which amplified subsequent mitogenesis.