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

被引:7
作者
EBIHARA, T [1 ]
KOYAMA, S [1 ]
机构
[1] UNIV TSUKUBA, INST CLIN MED, DEPT INTERNAL MED, TSUKUBA 305, JAPAN
关键词
RIL-2; TCGF; MALIGNANT ASCITES; LAK; CTL;
D O I
10.1620/tjem.162.49
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 (rIL2) 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. TCFG-activated EAL cells acquired higher anti-Daudi tumor cytotoxicity than rIL 2-activated EAL cells. The resultant TCFG-activated EAL cells from cancer patients significantly exceeded lytic activity of TCFG-activated EAL cells from patient with liver cirrhosis for control (p < 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 TCFG 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+ CDl1- and CD8+CD28+ effector cells.
引用
收藏
页码:49 / 63
页数:15
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