Inhibition of phosphatidylserine synthesis induced by triggering CD2 or the CD3-TCR complex in a human t cell line. Relationships with G proteins and receptors modulation

Abstract

Activation of Jurkat T cells with phytohemagglutinin, CD3 or CD2 mAbs results in a marked inhibition of phosphatidylserine (PS) synthesis. Monitoring PS synthesis in T cells shows that: (i) after modulation of CD3 molecules the cells become refractory to further treatment with CD3 mAbs as well as to a further challenge with CD2 mAbs; and (ii) treatment of T cells with fluoride ions and cholera toxin, two known effectors of guanosine trisphosphate-binding proteins, also resulted in a strong inhibition of the synthesis of this phospholipid. The inhibition of PS synthesis thus appears to be regulated similarly to the other activation events, suggesting that transmembrane signalling mechanisms leading to PS inhibition are the same as those previously proposed for increasing phosphatidylinositides turnover and subsequent rise in the intracellular calcium concn in lymphocytes.