Fransen L, Van der Heyden J, Ruysschaert R, Fiers W
Eur J Cancer Clin Oncol. 1986 Apr;22(4):419-26. doi: 10.1016/0277-5379(86)90107-0.
Tumor Necrosis Factor (TNF), released by induced macrophages, causes tumor necrosis in animals, and preferentially kills transformed cells in vitro. Using pure, recombinant human TNF, we report here its cytotoxic action on several human transformed and non-transformed cell lines. Furthermore, remarkable synergism between TNF and interferon-gamma (IFN-gamma) was observed in a large number of human cell lines, especially breast, cervix and colon carcinomas. Some other human cell lines, not sensitive to TNF alone, became highly sensitive when IFN-gamma was present as well. We could not demonstrate a synergism between TNF and IFN-gamma on any of the lymphoma/leukemia cell lines tested. All normal human, non-transformed diploid cell lines were insensitive to TNF even in the presence of IFN-gamma. This study also confirms the observation that inhibition of protein synthesis by metabolic drugs (e.g. actinomycin D) remarkably enhances the sensitivity of several target cell lines to cytolysis by TNF.
由诱导的巨噬细胞释放的肿瘤坏死因子（TNF）可导致动物体内肿瘤坏死，并在体外优先杀死转化细胞。我们使用纯的重组人TNF，在此报告其对几种人转化细胞系和未转化细胞系的细胞毒性作用。此外，在大量人细胞系中，尤其是乳腺癌、宫颈癌和结肠癌细胞系中，观察到TNF与干扰素-γ（IFN-γ）之间存在显著的协同作用。其他一些单独对TNF不敏感的人细胞系，当同时存在IFN-γ时则变得高度敏感。在我们测试的任何淋巴瘤/白血病细胞系中，均未证明TNF与IFN-γ之间存在协同作用。即使存在IFN-γ，所有正常的人未转化二倍体细胞系对TNF均不敏感。本研究还证实了以下观察结果：代谢药物（如放线菌素D）对蛋白质合成的抑制作用可显著增强几种靶细胞系对TNF细胞溶解作用的敏感性。
