The effect of prenatal exposure to cyclophosphamide on postnatal somatic development and the function of the immune system was studied in random-bred ICR mice. In a dose of 1.2 mg (i.e. an average of 23.5 mg/kg pregnant female body weight), cyclophosphamide administered on the 16th day of gestation (a vaginal plug = day 1) caused both prenatal and postnatal retardation of growth. In the 3rd, 5th and 8th postnatal week, increased proliferation of the splenocytes of the experimental mice was observed in vitro, with changes in the intensity of their activation by Concanavalin A and lipopolysaccharide. In the 3rd week their capacity for activation by lipopolysaccharide was markedly lower than their activation by Concanavalin A and phytohaemagglutinin. No differences were observed between proliferation and activation of the splenocytes of the offspring of the control and the experimental mice at the age of 16 weeks. After depression at three weeks, the delayed type hypersensitivity reaction showed a tendency to increase; in the offspring of the experimental mice the haemagglutinin titre against sheep RBC was raised during the whole period of the investigation. At 16 weeks, the activity of peritoneal macrophages was likewise elevated.