Yanase M, Tsukamoto T, Kumamoto Y, Kato K, Hashimoto Y
Department of Urology, Sapporo Medical University, Japan.
Cancer Immunol Immunother. 1994 Jul;39(1):22-6. doi: 10.1007/BF01517176.
Recent studies have shown that cytokine treatment of tumor cells alters the sensitivity of these cells to lymphokine-activated killer (LAK) cells, depending on the cell line. In this study, we analyzed the decrease in LAK sensitivity of a human renal-cell carcinoma cell line (SMKT-R-3). The LAK sensitivity of SMKT-R-3 was decreased by treatment with a combination of interferon gamma (IFN gamma) and tumor necrosis factor (TNF). However, the cytokine treatment increased the expression of intercellular adhesion molecule-1 (ICAM-1) on the renal-cell carcinoma cell surface. The conjugate-formation assay also confirmed a slight increase in the binding rate of LAK cells to the renal-cell carcinoma cells. When actinomycin D (a protein synthesis inhibitor) was added to the culture medium prior to treatment with IFN gamma and TNF, the LAK sensitivity of SMKT-R-3 recovered to the level demonstrated by the cells that had not received any cytokine treatment. These results suggest that the effect of cytokines in reducing LAK sensitivity of SMKT-R-3 is mediated by protein synthesis occurring when LAK cells are bound to SMKT-R-3 cells.
最近的研究表明，细胞因子对肿瘤细胞的处理会改变这些细胞对淋巴因子激活的杀伤细胞（LAK细胞）的敏感性，具体情况取决于细胞系。在本研究中，我们分析了一种人肾癌细胞系（SMKT-R-3）对LAK细胞敏感性的降低情况。用γ干扰素（IFNγ）和肿瘤坏死因子（TNF）联合处理降低了SMKT-R-3对LAK细胞的敏感性。然而，细胞因子处理增加了肾癌细胞表面细胞间黏附分子-1（ICAM-1）的表达。共轭形成试验也证实了LAK细胞与肾癌细胞结合率略有增加。在用IFNγ和TNF处理之前，向培养基中加入放线菌素D（一种蛋白质合成抑制剂）后，SMKT-R-3对LAK细胞的敏感性恢复到未接受任何细胞因子处理的细胞所显示的水平。这些结果表明，细胞因子降低SMKT-R-3对LAK细胞敏感性的作用是由LAK细胞与SMKT-R-3细胞结合时发生的蛋白质合成介导的。
