Ward S G, Cantrell D A
Lymphocyte Activation Laboratory, Imperial Cancer Research Fund, London, England.
J Immunol. 1990 May 1;144(9):3523-8.
In many cells, protein kinase C (PKC) activation inhibits cellular phospholipase C thereby preventing receptor-mediated phosphatidylinositol (PI) metabolism. In T lymphocytes, the T cell antigen receptor (Ti)/CD3 complex regulates PI hydrolysis and we have examined the consequences of PKC activation on Ti/CD3-mediated PI metabolism in human peripheral blood-derived T lymphocytes (T lymphoblasts) and the leukemic T cell line Jurkat. In Jurkat cells, PI metabolism after Ti/CD3 stimulation, is inhibited by PKC activation. PKC activation also inhibits calcium-induced PI metabolism in permeabilized Jurkat cells. In marked contrast, PI metabolism after Ti/CD3 stimulation in T lymphoblasts, is not inhibited by PKC activation. Moreover, in permeabilized T lymphoblasts PI metabolism can be induced by calcium in synergy with guanine 5'-O-(3-thiotrisphosphate) via a PKC-insensitive mechanism. The different effect of PKC stimulation on PI metabolism in Jurkat cells and T lymphoblasts reveals heterogeneity of PLC regulation in T lymphocytes. The data also indicate that the role of PKC as a regulator of Ti/CD3 signal transduction can differ depending on cell type.
在许多细胞中，蛋白激酶C（PKC）的激活会抑制细胞磷脂酶C，从而阻止受体介导的磷脂酰肌醇（PI）代谢。在T淋巴细胞中，T细胞抗原受体（Ti）/CD3复合物调节PI水解，我们已经研究了PKC激活对人外周血来源的T淋巴细胞（T淋巴母细胞）和白血病T细胞系Jurkat中Ti/CD3介导的PI代谢的影响。在Jurkat细胞中，Ti/CD3刺激后的PI代谢受到PKC激活的抑制。PKC激活还抑制了通透化Jurkat细胞中钙诱导的PI代谢。与之形成显著对比的是，T淋巴母细胞中Ti/CD3刺激后的PI代谢不受PKC激活的抑制。此外，在通透化的T淋巴母细胞中，PI代谢可通过与鸟嘌呤5'-O-（3-硫代三磷酸）协同作用的钙，经由一种PKC不敏感机制诱导产生。PKC刺激对Jurkat细胞和T淋巴母细胞中PI代谢的不同影响揭示了T淋巴细胞中PLC调节的异质性。这些数据还表明，PKC作为Ti/CD3信号转导调节因子的作用可能因细胞类型而异。
