The physiological protection from fetal rejection is believed to be dependent on a Th2 type of inflammatory response at the maternal-fetal interface and the cytokines IL-4 and IL-10 have been suggested to play a critical role. We here present data from breeding experiments with IL-10 and IL-4 double-deficient mice indicating that neither maternal nor feto-placental deficiency of these cytokines are crucial for fetal or neonatal survival. The present study does not analyse possible developmental effects of maternal or fetal IL-10 and IL-4 double-deficiency in detail, but shows that an apparently normal breeding can be achieved in different crossings, providing that the mice are kept under very clean conditions.