Stoeck M, Howe R C, Miescher S, von Fliedner V, MacDonald H R
Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges, Switzerland.
Immunobiology. 1990 Aug;181(1):13-21. doi: 10.1016/s0171-2985(11)80161-0.
In order to further characterize the action of transforming growth factor beta (TGF-beta) on lymphoid cells, we investigated the effects of porcine TGF-beta 1 and -2 on the IL-1 sensitive EL4/6.1 thymoma cell line. The proliferation of EL4/6.1 thymoma cells was inhibited by TGF-beta 1 and TGF-beta 2 (1 ng/ml) to a similar degree, the population doubling time was increased by 50-60%, total inhibition was not achieved. This decrease of proliferation was associated with an increase of the number of cells in the G0/G1 compartment of the cell cycle. TGF-beta-mediated inhibition could not be overcome by adding exogenous rIL-1 nor was the binding capacity for IL-1 reduced. In addition, TGF-beta did not interfere with the induction of IL-2 receptors by a combination of Ionomycin+PMA+IL-1. The data suggest that TGF-beta mediated inhibition of thymocyte/lymphocyte proliferation is not associated with an inhibition of the expression or the induction of expression of IL-2 or IL-1 receptors.
为了进一步描述转化生长因子β（TGF-β）对淋巴细胞的作用，我们研究了猪TGF-β1和-2对IL-1敏感的EL4/6.1胸腺瘤细胞系的影响。TGF-β1和TGF-β2（1 ng/ml）对EL4/6.1胸腺瘤细胞增殖的抑制程度相似，群体倍增时间增加了50-60%，但未实现完全抑制。这种增殖的减少与细胞周期G0/G1期细胞数量的增加有关。添加外源性rIL-1不能克服TGF-β介导的抑制作用，IL-1的结合能力也未降低。此外，TGF-β不干扰离子霉素+佛波酯+IL-1联合诱导IL-2受体。数据表明，TGF-β介导的胸腺细胞/淋巴细胞增殖抑制与IL-2或IL-1受体表达的抑制或诱导表达无关。
