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首页> 外文期刊>Molecular and Cellular Biology >Inhibition of T-cell antigen receptor-mediated transmembrane signaling by protein kinase C activation.
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Inhibition of T-cell antigen receptor-mediated transmembrane signaling by protein kinase C activation.

机译：蛋白激酶C激活抑制T细胞抗原受体介导的跨膜信号传导。

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The murine T-lymphoma cell line LBRM-33 is known to require synergistic signals delivered through the antigen receptor (Ti-CD3) complex, together with interleukin 1 (IL-1), for activation of IL-2 gene expression and IL-2 production. Although 12-O-tetradecanoylphorbol-13-acetate (TPA) was capable of replacing IL-1 as an activating stimulus under certain conditions, biologic studies indicated that TPA failed to synergize with Ti-CD3-dependent stimuli under conditions in which IL-1 was clearly active. Acute exposure to TPA and other active phorbol esters resulted in a concentration-dependent inhibition of the increases in phosphoinositide hydrolysis and intracellular free Ca2+ concentration stimulated by phytohemagglutinin or anti-Ti antibodies. TPA treatment induced no direct alteration of phospholipase C enzymatic activities in LBRM-33 cells. In contrast, both Ti-CD3 cross-linkage and TPA rapidly stimulated the phosphorylation of identical CD3 complex polypeptides, presumably via activation of protein kinase C. Exposure of LBRM-33 cells to TPA resulted in a time-dependent, partial down-regulation of surface Ti-CD3 expression. Thus, TPA treatment inhibited the responsiveness of LBRM-33 cells to Ti-CD3-dependent stimuli by inducing an early desensitization of Ti-CD3 receptors, followed by a decrease in membrane receptor expression. These studies indicate that phorbol esters deliver bidirectional signals that both inhibit Ti-CD3-dependent phosphoinositide hydrolysis and augment IL-2 production in LBRM-33 cells.
机译：已知鼠T淋巴瘤细胞系LBRM-33需要通过抗原受体（Ti-CD3）复合物以及白介素1（IL-1）传递协同信号来激活IL-2基因表达和IL-2生产。尽管在某些条件下12-O-十四烷酰phorbol-13-乙酸盐（TPA）能够代替IL-1作为激活刺激，但生物学研究表明，在IL-1的条件下，TPA无法与Ti-CD3依赖性刺激协同作用显然很活跃。急性暴露于TPA和其他活性佛波酯会导致浓度依赖性抑制植物血凝素或抗Ti抗体刺激的磷酸肌醇水解和细胞内游离Ca 2+浓度的增加。 TPA处理不会在LBRM-33细胞中诱导磷脂酶C酶活性的直接改变。相比之下，Ti-CD3交联和TPA都能迅速刺激相同CD3复合多肽的磷酸化，大概是通过激活蛋白激酶C来实现的。LBRM-33细胞暴露于TPA会导致时间依赖性，部分下调Ti-CD3表面表达。因此，TPA处理通过诱导Ti-CD3受体早期脱敏，然后减少膜受体表达，从而抑制LBRM-33细胞对Ti-CD3依赖性刺激的反应性。这些研究表明佛波酯可传递双向信号，既抑制Ti-CD3依赖性磷酸肌醇水解，又增加LBRM-33细胞中IL-2的产生。

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