Abstract
Blood leukocytes, spleen, bone marrow, and fetal liver cells from strains of mice that respond well (HR) or poorly (LR) to the synthetic polypeptide (T,G)-A—L were challenged in vitro with this antigen. At the peak of the response, there were 2 to 100 times more HR than LR blood, spleen, and marrow cells proliferating; however, there was no detectable difference when stem cells from HR and LR embryos were stimulated. An antiserum to the ϑ antigen greatly reduced the responses to (T,G)-A—L of HR and LR blood, spleen, and marrow cells; this antiserum had no effect on the response by cells from fetal liver. Spleen-incubated HR thymus cells were more effective than similarly treated cells from LR mice in increasing the proliferation of fetal lymphoid cells challenged with (T,G)-A—L. The results suggest that LR strains respond poorly to (T,G)-A—L because of an antigen-induced cell membrane change that affects primarily the function of the thymus-passaged cell; this change impedes contact between thymus-passaged cells and the specific antibody-producing precursors with the result that proliferation and/or recruitment of the latter is impaired.

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