Immunological memory in radiation chimeras.

Humoral antibody formation in the long-term allogeneic radiation chimera was found to be dependent upon the type and dose of antigen and the degree of secondary disease experienced. The antigen most capable of revealing a defect in the immunological mechanism of these murine chimeras was rat red blood cells (RBC), a phylogenetically closely related antigen. Thus, two different allogeneic chimera combinations, with contrasting incidence and severity of secondary disease, failed to mount significant antibody titers to rat RBC even after repeated immunizations. Sheep RBC and Salmonella typhosa antigens, although evoking a subnormal response after primary immunization, were capable of inducing normal antibody titers after two or more injections. The consistent immunological defect, independent of antigen type, dose, and incidence of secondary disease, was the inability of these animals to show normal conversion from 19 S to 7 S antibody synthesis. On this basis we speculate that the deficiency in the allogeneic chimera lies in the T cell component of the immune system, since 7 S antibody formation has been shown by others to be a thymus-dependent function.