Lysis of fresh natural killer-resistant tumor cells by lectin-activated syngeneic and allogeneic murine splenocytes.

This paper demonstrates that lectin-activated lymphocytes of selected mouse strains can lyse fresh autologous or allogeneic tumor cells but not the fresh normal cells tested in short-term 51Cr release assays. Murine splenocytes, incubated with concanavalin A for 3 days, lysed tumor cells from fresh syngeneic P815 mastocytoma, 102 methylcholanthrene sarcoma, and FBL3 lymphoma; fresh allogeneic 3LL lung carcinoma and MethA sarcoma; and tissue-cultured YAK cells in 18-hr51Cr release assays. Natural killer cells in fresh splenocyte preparations only lysed tissue-cultured YAK cells and not the other targets. Syngeneic and allogeneic lymphoblasts, lung, or liver cells were not lysed by the concanavalin A-activated killer (CAK) cells. The induction of cytotoxicity by concanavalin A incubation was abrogated by alpha-methylmannoside in the 3-day incubation, but not in cytotoxicity assay. Radiosensitive cells and adherent cells were necessary for the generation of CAK cells. The CAK effectors themselves were radioresistant, nonadherent, and mostly Thy 1+ and Ly 2+. The CAK phenomenon may be mediated by lymphokine production by an Ly 1+ cell, since depletion of Ly 1+ cells prior to activation abrogates CAK induction, and the ability of numerous mouse strains (and nude mice) to generate CAK cells correlated with their ability to produce Interleukin 2. The biological and therapeutic role of these cells is currently being investigated in murine syngeneic primary and metastatic tumor models.