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Immune Regulation by Platelet‐Activating Factor: II. Mediation of Suppression by Cytokine‐Stimulated Endothelial Cells In Vitro
Author(s) -
Lacasse Chantal,
RolaPleszczynski Marek
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.49.3.245
Subject(s) - tumor necrosis factor alpha , cytokine , biology , peripheral blood mononuclear cell , monocyte , immunology , platelet activating factor , umbilical vein , immune system , population , endocrinology , lymphocyte , medicine , in vitro , biochemistry , environmental health
Human umbilical vein endothelial cells (EC) can respond to endotoxin or to the inflammatory cytokines tumor necrosis factor (TNF) and interleukin 1 (IL‐1) by producing platelet‐activating factor (PAF). When EC were preexposed to TNF‐α (25 U/ml) for 1 h, and then washed, their subsequent coculture with peripheral blood mononuclear cells (PBMC) resulted in suppressed proliferative response of the latter to the mitogen Con A ( P < 0.05). This effect was completely reversed by the concomitant use of the PAF receptor antagonist BN 52021 (0.1 mM). Preexposure of EC to IL‐1β (0.5 U/ml) induced similar effects, but IL‐1 and TNF were not additive. Removal of monocytes from the PBMC population abolished the effects. On the other hand, coculture of monocytes with cytokine‐preexposed EC resulted in significant induction of suppressor activity on lymphocyte proliferation. Our data indicate that EC, preexposed to inflammatory cytokines, can modulate lymphocyte functions via the production of PAF and its action on monocytes.