[Abstract] [Full Text PDF] (in Japanese / 807KB) [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 94(8): 781-790, 1993


Original article

FUNCTIONAL AND PHENOTYPIC ANALYSIS OF TUMOR INFILTRATING LYMPHOCYTES DERIVED FROM SOLID TUMORS AND EFFUSION ASSOCIATED LYMPHOCYTES IN MALIGNANT ASCITES CULTURED IN RECOMBINANT INTERLEUKIN 2

1) First Department of Surgery, Tohoku University School of Medicine, Sendai, Japan
2) Department of Surgery, lwaki Kyoritsu General Hospital, Iwaki, Japan
3) Department of Surgery, Tohoku Rosai Hospital, Sendai, Japan

Kazuhiro Itoh1)2), Kenichi Shiiba1), Nobuo Ebina1), Ryoichi Anzai1), Akio Ouchi1)3), Seiki  Matsuno1)

Tumor infiltrating lymphocytes (TIL) and effusion associated lymphocytes (EAL) were isolated from 7 human solid tumors and 6 malignant ascitic fluids respectively, and cultured in rIL2 (700JRU/ml)-containing medium. Long-term culture (> 14 days) of separated lymphocytes with exponential increase in cell number was achieved in 5 EAL-cultures, whereas in only 2 TIL-cultures. rIL2-expanded TIL and EAL manifested significant cytotoxicity in a 4-hrs chronium release assay. The maximun NK and LAK activity were reached 21 days and 14 days after starting incubation with rIL2 respectively, followed by a rapid decrease in cytolytic potential without declining growth rate of the cells. Phenotypic analysis showed the majority of the freshly isolated TIL and EAL were CD3+ T cells, and CD16+ NK cells were rarely identified in TIL. With induction of LAK cell activity, CD8+ T cells predominantly increased in TIL-cultures, while both CD4+ and CD8+ T cells and CD16+ NK cells were increased in EAL cultures. In activated TIL most cytolytic activity was found in CD8+T cells, in contrast CD16+ NK cells were responsible for it in activated EAL.
These results indicated that EAL and TIL have similar properties in which they coexist with cancer cells at tissue level and were capable of expanding and acquiring LAK cell activity in the presence of rIL2, but apparently differ in their mechanism of rIL2-mediated activation.


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