Experiments were carried out to assess the role of naturally acquired antibody-specific immunoregulation in the immunodeficiency of aged individuals. It was found that greater than 50% of the primary dinitrophenyl-specific BALB/c B cells did not respond in carrier-primed 2-yr-old BALB/c adoptive hosts as compared with similarly primed younger recipients. Similar suppression was observed in carrier-primed younger BALB/c mice that had received 4 x 10(7) spleen cells from 2-yr-old BALB/c mice, as opposed to those that had received 4 x 10(7) spleen cells from younger mice. This diminution in responsiveness was noted only for syngeneic BALB/c B cells because B cells of strains differing from BALB/c in the heavy chain allotype-idiotype locus were not suppressed. These findings indicate that old, but not young, mice had developed the capacity to suppress primary B cells bearing receptors expressing much of the syngeneic antibody repertoire. This suppression may play an important causative role in the relatively poor humoral immune responsiveness of aged individuals.
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