IL-1 signaling for IL-2 production in T cells involves a rise in phosphatidylserine synthesis.
IL-1 signaling for IL-2 production in T cells involves a rise in phosphatidylserine synthesis.
复制标题
T 细胞中 IL-2 产生的 IL-1 信号传导涉及磷脂酰丝氨酸合成的增加。
作者：
M. Didier;C. Aussel;C. Pelassy;M. Fehlmann
具有抗tcr、抗cd3、抗cd2或PHA的Jurkat T细胞的激活伴随着对磷脂酰丝氨酸（PS）合成的强烈抑制。IL-1可部分逆转对该磷脂合成的抑制作用。在Jurkat细胞中，IL-1不激活磷酸二酯酶，这可以通过肌醇三磷酸和二酰基甘油水平的变化以及细胞质Ca2+浓度的变化来证明。此外，IL-1并没有改变细胞内cGMP和cAMP的水平，表明所观察到的PS合成的升高可能起到了IL-1的中介作用。由于PS是蛋白激酶C激活的必要辅助因子，我们的研究结果强烈提示IL-1通过其对PS合成的作用来调节活化淋巴细胞中蛋白激酶C的活性。
Activation of Jurkat T cells with anti-TCR, anti-CD3, anti-CD2, or PHA is accompanied by a strong inhibition of phosphatidylserine (PS) synthesis. The inhibition of the synthesis of this phospholipid could be partially reversed by IL-1. In Jurkat cells, IL-1 did not activate phosphodiesterases as demonstrated by the lack of change of inositol triphosphate and diacylglycerol levels as well as the lack of change in cytosolic Ca2+ concentration. Furthermore, IL-1 did not modify the intracellular level of cGMP and cAMP, suggesting that the observed rise of PS synthesis could play the role of mediator IL-1 action. As PS is a necessary cofactor for the activation of protein kinase C, our results suggest strongly that IL-1 modulate protein kinase C activity in the activated lymphocyte through its action on PS synthesis.