The mechanism of specific suppression in effector T cell clones against tumor-associated transplantation antigens.

The present study investigates the fate of effector T cell population against tumor-associated transplantation antigens (TATA) of X5563 plasmacytoma in syngeneic mice rendered specifically unresponsive to the TATA. In this tumor system T cell-mediated tumor-specific immunity was induced by intradermal inoculation of viable tumor cells followed by the surgical resection of the tumor (immunization procedure). The intravenous (iv) presensitization of syngeneic hosts with X-irradiated tumor cells abolished the capability of those hosts to develop the tumor-specific immunity after the above appropriate immunization procedure. Spleen cells from the pretreated mice which subsequently received the immunization procedure could not regain the tumor-neutralizing activity after enzymatic treatment with papain. Moreover, lymphoid cells from the pretreated mice could not be stimulated by the immunization procedure even after proteolytic treatment with papain or trypsin, followed by transfer into other recipient mice free of the serum suppressive factor(s). On the other hand, such enzyme treatment was capable of preventing the tolerance induction of dinitrophenyl (DNP)-primed B cells after in vitro pulsing with DNP-D-GL (copolymer of D-glutamic acid and D-lysine) for 2 hr, suggesting that the enzymatic treatment used here was adequate to remove the blocked receptor and any tolerogen. These results suggest that in X5563 plasmacytoma system, the above specific unresponsiveness induced by the iv presensitization with TATA is due to the irreversible inhibition or deletion of effector T cell clones rather than mere effector cell blockade.