Biffen M, Shiroo M, Alexander D R
AFRC Babraham Institute, Cambridge, GB.
Eur J Immunol. 1993 Nov;23(11):2980-7. doi: 10.1002/eji.1830231138.
In HPB-ALL T-cells the p59fyn tyrosine kinase is regulated by the CD45 phosphotyrosine phosphatase and plays a critical role in coupling the T cell receptor (TCR) to the generation of intracellular signals which include diacylglycerol (DAG) production and protein kinase C activation. The aim of this study was to determine the phospholipid pools from which the DAG is generated and to identify which phospholipase activities are regulated by the TCR. When CD45+ cells were pre-labeled with [3H]arachidonic acid, CD3-antigen cross-linking stimulated negligible increases in both [3H]DAG and [3H]phosphatidic acid (PA). However, CD3 monoclonal antibody (mAb) induced an increase of 300% in [3H]PA when the cells were permeabilized with streptolysin-O, and this correlated with increased levels of protein tyrosine phosphorylation. Stimulation of [3H]PA production upon CD3 cross-linking was 77% lower in permeabilized CD45- cells than in CD45+ cells, consistent with the reduced activity of p59fyn in CD45- cells. The stimulated production of PA was not mediated by activation of phospholipase D (PLD), although the presence of a G-protein-regulated PLD activity was established. The CD3-induced increase in total inositol phosphates (InsP) in permeabilized cells was similar to the stimulated production of [3H]PA production in both CD45+ and CD45- cells. Dose-response curves for InsP and PA production triggered by CD3 mAb were super-imposable and the production of InsP and PA over a range of Ca2+ concentrations was comparable. Differential labeling of phospholipids with 3H-labeled fatty acids revealed that CD3-induced PA production reflected incorporation of label into the phosphatidylinositol pool. Our data suggest that in HPB-ALL cells the production of DAG following CD3-antigen cross-linking can be fully accounted for by the selective coupling of the TCR to breakdown of phosphatidylinositol-(4,5)-bisphosphate as the result of phospholipase C gamma 1 activation. This event correlates with the activity of the CD45-regulated TCR-associated tyrosine kinase, p59fyn.
在人外周血B淋巴细胞来源的急性淋巴细胞白血病(HPB-ALL)T细胞中,p59fyn酪氨酸激酶受CD45磷酸酪氨酸磷酸酶调控,在将T细胞受体(TCR)与包括二酰基甘油(DAG)生成和蛋白激酶C激活在内的细胞内信号产生相偶联过程中起关键作用。本研究的目的是确定产生DAG的磷脂池,并鉴定哪些磷脂酶活性受TCR调控。当用[3H]花生四烯酸对CD45+细胞进行预标记时,CD3抗原交联刺激后,[3H]DAG和[3H]磷脂酸(PA)的增加可忽略不计。然而,当用链球菌溶血素-O使细胞通透后,CD3单克隆抗体(mAb)诱导[3H]PA增加300%,这与蛋白酪氨酸磷酸化水平升高相关。CD3交联后,通透的CD45-细胞中[3H]PA的产生比CD45+细胞低77%,这与CD45-细胞中p59fyn活性降低一致。尽管已证实存在G蛋白调节的磷脂酶D(PLD)活性,但PA的刺激产生并非由PLD激活介导。CD3诱导的通透细胞中总肌醇磷酸(InsP)增加与CD45+和CD45-细胞中[3H]PA产生的刺激情况相似。CD3 mAb触发的InsP和PA产生的剂量反应曲线相互叠加,并且在一系列Ca2+浓度范围内InsP和PA的产生相当。用3H标记的脂肪酸对磷脂进行差异标记显示,CD3诱导的PA产生反映了标记物掺入磷脂酰肌醇池。我们的数据表明,在HPB-ALL细胞中,CD3抗原交联后DAG的产生可完全归因于TCR与磷脂酰肌醇-(4,5)-二磷酸的分解选择性偶联,这是磷脂酶Cγ1激活的结果。该事件与CD45调节的TCR相关酪氨酸激酶p59fyn的活性相关。