The suppressor T cell (Ts) function of old NZW, NZB, C57BL/6 and (NZB X NZW) F1 [B/W)F1), mice to the 2,4-dinitro-1-fluorobenzene (DNFB) hapten was studied. Intravenous administration of dinitrophenyl (DNP) coupled syngeneic lymphoid cells (which normally induce DNP specific suppression) did not result in suppression of DNFB-specific contact hypersensitivity (CS) responses in old NZB or (B/W) F1 mice. Nevertheless, when spleen cells from these old mice were injected into young mice (either (B/W)F1 or A/Sn), strong suppression of the induction phase of CS responses was observed. In addition, effector phase suppressor activity was also observed when splenic cells from tolerized old (B/W) F1 donors were transferred into young (B/W)F1 mice during the effector phase of the CS response. In both cases, the significant cells in the transfer were I-J+ T cells. Thus, the old mice retained functional Ts1 and Ts2 suppressor cells. However, the suppressive activity of the old mice could be reconstituted with spleen cells from primed young mice, suggesting that they have a defect in the Ts3 subset. This was further supported by the finding that the significant cells from the primed young mice were I-J positive and cyclophosphamide-sensitive.