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Summary The effect of estrogenic hormones on survival and immunity was studied in sublethally irradiated, lethally irradiated and syngeneic bone marrow transplanted, and nonirradiated mice. When either estradiol or estriol were administered for 2 weeks after x-irradiation, excessive early mortality occurred. Evaluation of the allograft and hemagglutinin responses in the animals surviving 4 weeks postirradiation revealed that the St. Luke's myeloma, indigenous to the C3H strain, injected into sublethally irradiated AKR mice grew progressively and killed the majority of the estrogen recipients, but regressed in the control-treated irradiated mice; first set allogeneic skin graft survival was prolonged by estradiol in sublethally irradiated mice and by both estrogens in lethally-irradiated recipients; and the primary hemagglutinin response to sheep red cells was markedly depressed by both agents in lethally-irradiated mice and by estradiol in sublethally-irradiated animals. By contrast, neither the survival nor the allograft or hemagglutinin responses were altered by estrogens in nonirradiated normal or pretreated mice. Finally, adoptive immunity was not influenced by hormonal treatment.

Summary The effect of donor or host immunologically competent cells added 21 days after lethal irradiation and allogeneic bone marrow transplantation was investigated in mice. Whereas 10 × 106 normal host lymphocytes or spleen cells had no effect on the subsequent course of secondary disease, 50 × 106 normal host spleen cells significantly improved survival. Normal donor cells were efficacious at both dosages, but particularly at the highest inoculum. Cells obtained from strains unrelated to the donor or host were either not effective or harmful. To test the susceptibility of the chimera 21 days after bone marrow transplantations, spleen cells preimmunized to either donor or host tissues were administered and found to be consistently destructive. The mechanism whereby large innocula of normal donor or host cells improve survival is unknown, but a hypothesis based on inhibition of the primary immune response by serum antibody if offered for consideration.