REGULATION OF INTERLEUKIN-2 PRODUCTION AND PHOSPHATIDYLSERINE SYNTHESIS IN JURKAT LYMPHOCYTES-T BY K+ CHANNEL ANTAGONISTS

被引:15
作者
AUSSEL, C [1 ]
PELASSY, C [1 ]
MARY, D [1 ]
CHOQUET, D [1 ]
ROSSI, B [1 ]
机构
[1] INST PASTEUR, INSERM, U261, NEUROBIOL CELLULAIRE LAB, F-75724 PARIS, FRANCE
来源
IMMUNOPHARMACOLOGY | 1990年 / 20卷 / 02期
关键词
Interleukin-2; production; K[!sup]+[!/sup] channel; Lymphocyte; Phosphatidylserine synthesis;
D O I
10.1016/0162-3109(90)90012-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Modification of phospholipid metabolism during T cell activation has been repeatedly reported. Recently, we have shown that phytohaemagglutinin, CD3 and CD2 mAbs, which are potent in vitro activators of helper T lymphocytes, markedly inhibit phosphatidylserine synthesis concomitantly as they induce the secretion of IL-2. In this paper, we show evidence that in T lymphocytes K+ channels, which have been shown to participate in the cell activation process, are also reciprocally related to phosphatidylserine synthesis. In fact, in resting T cells the drugs affecting the activity of K+ channels, such as quinine and 4-aminopyridine, induce a rise of phosphatidylserine synthesis. In activated cells, quinine and 4-aminodopyridine also caused a rise in phosphatidylserine synthesis which paralleled a decreased production of IL-2, strongly suggesting that these two events are correlated in a reciprocal manner. More precisely, phosphatidylserine synthesis was stimulated by drugs which have been reported to inhibit potassium channels in lymphocytes, e.g. quinine, 4-aminopyridine, tetraethylammonium. These data suggest that the decreased PS synthesis observed during T cell activation intervenes in the cascade of events leading to IL-2 secretion. The decrease in the biosynthesis of this phospholipid seems to be dependent on the activity of K+ channels. © 1990.
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页码:97 / 103
页数:7
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