Spleen cells from mice primed previously with keyhole limpet hemocyanin (KLH), horse erythrocytes (HRBC) or trinitrophenyl (TNP)-HRBC were incubated in vitro under appropriate conditions and with doses of anti-immunoglobulin antibodies known to cause partial or complete endocytosis of surface Ig-anti-Ig complexes. The effect of such treatment on the immune capacity of such cells was evaluated by both in vivo adoptive transfer secondary antibody responses and in vitro secondary antibody responses. These studies have shown that movement and endocytosis of surface Ig receptors by anti-Ig do not, per se, diminish or abolish the capacity of primed lymphoid cells to respond in a normal fashion to antigen subsequent to the reappearance of their receptors. Similarly, movement and endocytosis, per se, do not appear to trigger primed B lymphocytes to result in antibody formation in the absence of specific antigen either in vivo or in vitro. On the other hand, after reaction with anti-Ig, the efficiency of the antibody response of primed lymphoid cells in vitro is significantly increased upon subsequent antigenic stimulation.

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