Functional and phenotypic characteristics of effusion-associated lymphoid cells cultured in the presence of either recombinant interleukin 2 or T-cell growth factor from malignant pleural and peritoneal effusions in patients with advanced carcinoma.

Malignant pleural or peritoneal effusion-associated lymphoid (EAL) cells from 17 patients with advanced carcinoma were cultured with autologous carcinoma cells in the presence of either recombinant interleukin 2 (rIL 2) or T-cell growth factor (TCGF). Considerable cytolytic activity of the cells against allogeneic tumor cells, such as K562 and Daudi cells was induced by the cultivation. TCGF-activated EAL cells acquired higher anti-Daudi tumor cytotoxicity than rIL 2-activated EAL cells. The resultant TCGF-activated EAL cells from cancer patients significantly exceeded lytic activity of TCGF-activated EAL cells from patients with liver cirrhosis for control (p less than 0.01). Four of 6 cases examined also showed cytotoxic activity against autologous tumor. In facts, viable carcinoma cells co-cultured with EAL cells and TCGF mostly disappeared during 14 days. Similar phenomenon was not observed in rIL 2-activated EAL cells. Thus, it was suggested that more additional lymphokine other than IL 2 was necessary to generate cytotoxic activity against autologous tumor cells. The cell populations responsible for cytolytic activity to allogeneic and/or autologous tumor cells were investigated by two-color flow cytometry. The majority of killer-effector cells against allogeneic cells in rIL 2-activated EAL cells from cancer patients showed CD4+Leu8- phenotype at population level. In contrast, it was suggested that cytolytic activity against allogeneic and/or autologous tumor cells in TCGF-activated EAL cells might be mediated by CD8+ CD11- and CD8+ CD28+ effector cells.