IL-1 signaling for IL-2 production in T cells involves a rise in phosphatidylserine synthesis.
Activation of Jurkat T cells with anti-TCR, anti-CD3, anti-CD2, or PHA is accompanied by a strong inhibition of phosphatidylserine (PS) synthesis. The inhibition of the synthesis of this phospholipid could be partially reversed by IL-1. In Jurkat cells, IL-1 did not activate phosphodiesterases as demonstrated by the lack of change of inositol triphosphate and diacylglycerol levels as well as the lack of change in cytosolic Ca2+ concentration. Furthermore, IL-1 did not modify the intracellular level of cGMP and cAMP, suggesting that the observed rise of PS synthesis could play the role of mediator IL-1 action. As PS is a necessary cofactor for the activation of protein kinase C, our results suggest strongly that IL-1 modulate protein kinase C activity in the activated lymphocyte through its action on PS synthesis.
Didier
M
M
INSERM U210, Faculté de Médecine (Pasteur), Nice, France.
Aussel
C
C
Pelassy
C
C
Fehlmann
M
M
D002460:Cell Line; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D007376:Interleukin-2 / Q000096:biosynthesis*; D008213:Lymphocyte Activation / Q000187:drug effects; D009712:Nucleotides, Cyclic / Q000378:metabolism; D010718:Phosphatidylserines / Q000096:biosynthesis*; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism*
D007375:Interleukin-1; D007376:Interleukin-2; D009712:Nucleotides, Cyclic; D010718:Phosphatidylserines; D010727:Phosphoric Diester Hydrolases