Functional and phenotypic characteristics of recombinant interleukin‐2 or T‐cell growth factor‐activated splenic lymphoid cells from patients with gastric or hepatocellular carcinoma

• Published in: Cancer 1990-09, Vol.66 (5), p.923-929
• Main Authors: Ebihara, Tsugio, Fukao, Katashi, Koyama, Shohei
• Format: Article
• Language: English
• Subjects: Adult; Aged; Antigens, Differentiation, T-Lymphocyte - analysis; Carcinoma, Hepatocellular - immunology; Carcinoma, Hepatocellular - pathology; CD4 Antigens - analysis; CD8 Antigens; Female; Humans; Immunity, Cellular; Interleukin-2 - pharmacology; Killer Cells, Lymphokine-Activated - cytology; Killer Cells, Lymphokine-Activated - immunology; Liver Neoplasms - immunology; Liver Neoplasms - pathology; Lymphocyte Activation - immunology; Male; Middle Aged; Phenotype; Spleen - cytology; Stomach Neoplasms - immunology; Stomach Neoplasms - pathology; T-Lymphocytes, Regulatory - cytology; T-Lymphocytes, Regulatory - immunology; Tumor Cells, Cultured - immunology; Tumor Cells, Cultured - pathology
• ISSN: 0008-543X; 1097-0142
• DOI: 10.1002/1097-0142(19900901)66:5<923::AID-CNCR2820660518>3.0.CO;2-R

Fourteen days' culture of human spleen cells with recombinant interleukin‐2 (rIL‐2) or T‐cell growth factor (TCGF) results in the generation of lymphokine‐activated killer (LAK) effector cells that have the unique property of lysing natural killer (NK) ‐resistant human tumor cells, Daudi, and NK‐sensitive K562 cells. LAK cells were generated from patients with advanced cancer or liver cirrhosis. The splenic LAK‐effector cell types were analyzed by two‐color flow cytometry. The rIL‐2‐induced LAK cells showed an increased proportion of CD8+CD11− and CD57+CD16− and a decreased proportion of CD4+Leu‐8− cells. In contrast, TCGF‐induced LAK cells revealed a significantly increased proportion of CD8+CD11− and CD4+Leu‐8− cells and a decreased proportion of CD57+CD16− cells. Thus, splenic LAK cells with different surface phenotypes were induced by the cultivation with rIL‐2 or TCGF. Furthermore, TCGF‐induced LAK cell activities in patients with cancer were found to be lower than the rIL‐2‐induced LAK cell activities. It was noted that the TCGF‐activated splenic lymphoid cells did not inhibit the effector process of tumor cell lysis by LAK cells that had been activated by rIL‐2. Other mechanisms of lower LAK cell activities of TCGF‐activated splenic lymphoid cells from patients with cancer were discussed. The findings suggest that spleens of examined patients with gastric or hepatocellular carcinoma do not seem to be responsible for suppression of cell‐mediated antitumor immunity.