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在1系豚鼠肝癌模型中证实的多种肿瘤细胞毒性的体外机制。

Multiple in vitro mechanisms of tumor cytotoxicity demonstrated in the line-1 guinea pig hepatoma model.

作者信息

Osteen R T, Piessens W F, David J R, Churchill W H

出版信息

J Natl Cancer Inst. 1975 Oct;55(4):873-8. doi: 10.1093/jnci/55.4.873.

Abstract

The line-1 guinea pig hepatoma was used to study in vitro tumor cytotoxicity. Cytotoxicity was determined by measurement of the loss of tritiated thymidine-labeled target cells from culture vessels. With this technique, we demonstrated that significant tumor cytotoxicity was caused by lymphoid cells from tumor-immune guinea pigs, by cells from guinea pigs immunized against an antigen urelated to the tumor target, and by cell-free supernatants rich in lymphocyte mediators. Addition of normal peritoneal exudate cells enhanced the cytotoxic potential of a small number of highly purified immune lymphocytes, which suggested that recruitment of normal cells is an additional mechanism of tumor cell death in this system.

摘要

使用1号线性豚鼠肝癌来研究体外肿瘤细胞毒性。通过测量来自培养容器中经氚标记胸腺嘧啶核苷标记的靶细胞的损失来确定细胞毒性。运用这项技术,我们证明了来自肿瘤免疫豚鼠的淋巴细胞、来自针对与肿瘤靶标无关的抗原免疫的豚鼠的细胞以及富含淋巴细胞介质的无细胞上清液会引起显著的肿瘤细胞毒性。添加正常腹膜渗出细胞可增强少量高度纯化免疫淋巴细胞的细胞毒性潜能,这表明募集正常细胞是该系统中肿瘤细胞死亡的另一种机制。

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