Lewis (L) rats treated with donor antigen [Lewis Brown-Norway (LBN) spleen cells] and antidonor antibody (L anti-BN serum) produce L anti-(L anti-BN) antibody that reaches peak titers 10 days later. The antiantibody functions as an antibody against cell-surface receptor molecules on Lewis recognition lymphocytes for BN antigen. LBN kidneys grafted at the time of peak antireceptor titer are not rejected and function indefinitely. Homeostasis of enhanced kidneys in long-term graft recipients was evaluted by four sets of experiments with the following results: (1) adoptive transfer of spleen cells from long-term recipients causes fatal graft-vs.-host disease in LBN and LDA hosts; (2) adoptive transfer of spleen cells from long-term recipients to new, otherwise untreated Lewis recipients of LBN kidneys delays rejection and prolongs recipient survival; (3) adoptive transfer of sensitized spleen cells to long-term recipients causes no apparent injury to enhanced LBN kidneys; (4) splenectomy in long-term recipients did not lead to deterioration of enhanced kidneys. It appears that long-term recipients maintain a delicate balance of effector and suppressor cells with respect to donor antigens.