Macrophage-secreted prostaglandin E sub(2) potentiates immune complex-induced B cell unresponsiveness

We used an in vitro murine model system to investigate how two types of accessory cells pulsed with immune complexes (IC) regulated B cell function. We demonstrate that IC-pulsed macrophages (M Phi ) induce hapten-specific B cell unresponsiveness, whereas IC-pulsed splenic lymphoid dendritic cells (LDC) and an LDC-like tumor line caused an augmentation of the antibody response. The mechanism by which IC-pulsed M Phi diminished antibody production required two signals. The first was an antigen-specific signal supplied by the IC, and the second a nonspecific co-factor which was a product of M Phi cyclo-oxygenase metabolism. Specifically, it was shown that prostaglandin E sub(2) (PGE sub(2)) could function as this co-factor.