Reactivity of human lymphocytes against autochthonous and allogeneic normal and tumor cells in vitro.

Human peripheral lymphocytes from tumor-bearing and non-tumor-bearing patients were added to monolayer cultures of autochthonous and allogeneic normal or neoplastic cells in vitro with or without phytohemagglutinin (PHA). The normal cells were derived from skin, the tumor cells from postnasal carcinomas or sarcomas. The cultures were scored for clearly visible plaques in the monolayer. Without PHA, lymphocytes affected autochthonous skin target cells in 1 of 16 cultures. If PHA was added,the figure increased to nearly 50%(12/28). Whether this phenomenon is related to an autoimmune reaction or to some less specific effect of the PHA stimulus is unknown at present. In the absence of PHA, lymphocytes from African tumor-bearing hosts destroyed allogeneic skin fibroblasts in 4 of 14 cases, and lymphocytes from non-tumor-bearing Swedish donors showed this effect in 14 of 24 tests. The somewhat lower reactivity of the African lymphocytes was also apparent in other tests. It cannot be stated whether the difference was due to the tumor-bearing condition of the hosts or to some other differences involved in comparison of the two groups. Without PHA, lymphocytes of the African tumor patients destroyed their own autochthonous tumor cultures in 4 of 16 cases. Addition of PHA increased the proportion of positives to 20 of 28. A comparison with the corresponding figures for autochthonous skin cultures (1/16 and 12/28, respectively) indicates a relatively higher reactivity against the autochthonous tumor cells, both with and without PHA. This cannot be interpreted as a difference in target cell sensitivity to the same lymphocyte action, because no such difference was apparent when the sensitivity of skin and tumor to allogeneic lymphocytes was compared in the absence of PHA (4/14 and 4/14 with African lymphocyte donors; 14/24 and 14/24 with Swedish lymphocyte donors, respectively). The most probable explanation is that the antigenic barrier responsible for the lymphocyte effect is larger for tumor than for skin, or that the results reflect a presensitization of the tumor donor against its autochthonous neoplastic cells.