Previous work has shown that in the mouse, pregnancy significantly increases the level of immunoglobulin secreting cells in the lymph nodes draining the uterus. In this report it is demonstrated that there is also a widely disseminated potentiating effect on levels of immune responsiveness. T-cell responses, manifest as bystander B-cell responses, T-dependent and T-independent B-cell responses to injected antigens and non-specific "responses" to injected mitogens, have all been shown to be potentiated. Ablation of the fetus with retention of a healthy placenta leads to a loss of the potentiating effect. Feeding pregnant mice on indomethacin results in a lowering of immunoglobulin-forming cell levels in the para-aortic lymph node but has no effect on the disseminated potentiation effect detected by the popliteal lymph node assay. It is concluded that the fetus or the placenta under direct control of the fetus, is the source of the "pregnancy factor" responsible for the disseminated potentiation effect, that this factor is unlikely to be a prostaglandin and that the B-cell is the likely target of the potentiating factor. The possible nature of the "factor" is discussed.