Abstract
The specificity of auto‐tumor cytotoxicity exerted by patients' T lymphocytes was investigated. Lymphocytes, both activated and non‐activated, were used as effectors against freshly separated tumor cells. Activation was achieved by treatment with interferon (Hu‐IFN‐α), stimulation with PHA, co‐cultivation with autologous tumor biopsy cells (ATS) and allogeneic lymphocytes (MLC). Of these activation systems, ATS was the most efficient in generating auto‐tumor cytotoxicity. In some cases the lymphocytes activated in MLC or treated with PHA also damaged autologous tumor cells, but IFN‐pretreatment of the lymphocytes had no such effect. When the ATS‐ or MLC‐activated lymphocytes were propagated with conditioned medium known to contain Interleukin‐2, their lytic potential against autologous tumors was maintained. In addition to autologous tumor biopsy cells, the effector populations were also confronted with other targets such as Con A blasts and allogeneic tumor biopsy cells. The latter were lysed by the lymphocytes activated in MLC, but not by the ATS cultures. Thus, on the population level, the ATS was specific for the autologous tumor cells. Cold target competition tests suggested that in the MLC‐s the autologous tumor cells were killed by a distinct set of lymphocytes because allogeneic cells (tumor cells or the stimulator lymphocytes), even if killed by the same effector populations, did not compete. Thus, in these cultures the auto‐tumor specificity of the lysis was on the level of the effector subset. Therefore, it is likely that, independently of the mode of activation, the auto‐tumor lysis is the function of lymphocytes which recognize tumor‐ or organ‐specific antigens on the target cells.