AbstractThe decline in antibody‐forming potential with age was studied in mice by analyzing the relative contributions of T and B cells in collaborative PFC responses to the T cell‐dependent antigens, dinitrophenylated (DNP) keyhole limpet hemocyanin, DNP‐human IgG, fowl IgG and sheep red blood cells. The experimental system involved the adoptive transfer of purified lymphocyte populations derived from the spleens of old and young mice into young irradiated recipients. An unequivocal reduction in B cell function was demonstrated in both primary and secondary antibody responses. In the former, young T cells failed to restore responsiveness to old B cells, while in the latter, similar results were obtained, even if old B cells were primed in the presence of young T cells. Despite the lower level of antibody production in old mice compared with young, no decrease in the number of antigen‐binding cells (detected by resetting and autoradiography) was observed. Taken together, these results suggest that a defect exists in B cells which is independent of T cell help, and that it is not due to cell depletion but rather to a qualitative abnormality in the cells themselves.Old T cells did not collaborate with young B cells as well as young T cells did, indicating a loss of helper T cell activity. Spleen cells from old mice, when mixed with young spleen cells at a 1:1 ratio, caused a reduction in their antibody‐forming potential which was consistent with the presence of cells with suppressive activity. The suppressor cells were shown to be T cells since their effect was abrogated by treatment with anti‐Thy‐1.2 serum plus complement and enriched by passage through nylon wool columns.These findings emphasize the need to use purified cell populations in analysis of responsiveness in old animals and highlight the multifactorial nature of the mechanisms involved in the a
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