Ujházy P, Maccubbin D, Eppolito C, Mihich E, Ehrke M J
Lymphokine Cytokine Res. 1994 Apr;13(2):99-106.
The role of tumor necrosis factor (TNF-alpha) on in vitro generation of lymphokine-activated killer (LAK) cells from murine thymocytes was investigated and compared to that on generation of LAK from splenocytes. TNF-alpha increased the potential of interleukin-2 (IL-2) at suboptimal concentrations to generate LAK activity in thymocytes even more than in splenocytes. In parallel, augmented [3H]thymidine uptake by thymocytes and splenocytes was seen. However, no net increase in viable cell number was observed. LAK effector cells from TNF-alpha plus IL-2 cultures responded with an increased [3H]thymidine uptake to restimulation by IL-2 alone. These results suggest that TNF-alpha + IL-2 may be inducing the expansion of a small subset of cells. NK1.1+ cells are a very minor subset of thymocytes, nevertheless phenotype analysis showed that in thymocytes, IL-2 + TNF-alpha generates NK1.1+ CD8- LAK effectors in contrast to NK1.1- CD8+ cells found with IL-2 alone. This result is consistent with the finding in the proliferation studies. The fact that thymocytes are stimulated by the TNF-alpha + IL-2 combination to proliferate as well as to develop a phenotypically distinct effector supports the role of TNF-alpha in intra- and extrathymic regulation.
研究了肿瘤坏死因子（TNF-α）对从小鼠胸腺细胞体外生成淋巴因子激活的杀伤细胞（LAK细胞）的作用，并与对从脾细胞生成LAK细胞的作用进行了比较。TNF-α在次优浓度下增强白细胞介素-2（IL-2）生成胸腺细胞中LAK活性的能力，甚至超过增强其生成脾细胞中LAK活性的能力。同时，观察到胸腺细胞和脾细胞的[3H]胸腺嘧啶核苷摄取增加。然而，未观察到活细胞数量的净增加。来自TNF-α加IL-2培养物的LAK效应细胞对单独用IL-2再刺激的反应是[3H]胸腺嘧啶核苷摄取增加。这些结果表明TNF-α + IL-2可能诱导一小部分细胞的扩增。NK1.1 +细胞是胸腺细胞中非常小的一个亚群，然而表型分析表明，在胸腺细胞中，IL-2 + TNF-α产生NK1.1 + CD8- LAK效应细胞，这与单独用IL-2时发现的NK1.1- CD8 +细胞形成对比。这一结果与增殖研究中的发现一致。TNF-α + IL-2组合刺激胸腺细胞增殖并发育出表型不同的效应细胞，这一事实支持了TNF-α在胸腺内和胸腺外调节中的作用。
