The Journal of Immunology, Vol 144, Issue 8 3123-3129, Copyright © 1990 by American Association of Immunologists

ARTICLES

Immunoregulatory functions of paf-acether. III. Down-regulation of CD4+ T cells high-affinity IL-2 receptor expression

A Dulioust, V Duprez, C Pitton, P Salem, A Hemar, J Benveniste and Y Thomas
INSERM U 200, Universite Paris-Sud, 32 rue des Carnets, Clamart, France.

In the present report, we further explored the mechanisms by which 1-O- alkyl-2-acetyl-sn-glycero-3-phosphocholine (paf-acether), a phospholipid mediator of inflammation inhibited PHA-induced CD4+ cell proliferation. Evidence was obtained that CD4+ cells stimulated with either PHA or immobilized OKT3 in the presence of paf at concentrations that block CD4+ cell proliferation, exhibited a marked decrease in high affinity IL-2R expression. Importantly, paf did not prevent the binding of IL-2 to its receptor. Scatchard analysis of the binding data indicated that paf caused more than 50% decrease in the number of IL-2 high affinity sites per cell, whereas the receptor ligand affinity remained essentially constant. Moreover, the down-regulation of high affinity IL-2R was also accompanied by a loss of IL-2-dependent proliferative capacity. Together these data suggest that decreased expression of high affinity IL-2R may contribute to the diminished proliferative activity observed in CD4+ cells stimulated with PHA or immobilized OKT3 in the presence of paf. They further emphasize the potential role of lipid proinflammatory mediators such as paf in the regulation of T cell activation.

This article has been cited by other articles:

				Y. Kihara, S. Ishii, Y. Kita, A. Toda, A. Shimada, and T. Shimizu Dual phase regulation of experimental allergic encephalomyelitis by platelet-activating factor J. Exp. Med., September 19, 2005; 202(6): 853 - 863. [Abstract] [Full Text] [PDF]