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胃癌或肝细胞癌患者的重组白细胞介素-2或T细胞生长因子激活的脾淋巴细胞的功能和表型特征

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

作者信息

Ebihara T, Fukao K, Koyama S

机构信息

Department of Internal Medicine, University of Tsukuba, Japan.

出版信息

Cancer. 1990 Sep 1;66(5):923-9. doi: 10.1002/1097-0142(19900901)66:5<923::aid-cncr2820660518>3.0.co;2-r.

Abstract

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.

摘要

用人重组白细胞介素-2(rIL-2)或T细胞生长因子(TCGF)对人脾细胞进行14天培养,可产生淋巴因子激活的杀伤(LAK)效应细胞,这些细胞具有裂解天然杀伤(NK)抗性人肿瘤细胞Daudi和NK敏感的K562细胞的独特特性。LAK细胞由晚期癌症或肝硬化患者产生。通过双色流式细胞术分析脾LAK效应细胞类型。rIL-2诱导的LAK细胞显示CD8 + CD11 -和CD57 + CD16 -细胞比例增加,CD4 + Leu - 8 -细胞比例降低。相比之下,TCGF诱导的LAK细胞显示CD8 + CD11 -和CD4 + Leu - 8 -细胞比例显著增加,CD57 + CD16 -细胞比例降低。因此,用rIL-2或TCGF培养可诱导出具有不同表面表型的脾LAK细胞。此外,发现癌症患者中TCGF诱导的LAK细胞活性低于rIL-2诱导的LAK细胞活性。值得注意的是,TCGF激活的脾淋巴细胞并不抑制rIL-2激活的LAK细胞对肿瘤细胞的裂解效应过程。还讨论了癌症患者中TCGF激活的脾淋巴细胞LAK细胞活性较低的其他机制。研究结果表明,所检查的胃癌或肝细胞癌患者的脾脏似乎不负责抑制细胞介导的抗肿瘤免疫。

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