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Functional activities of receptors for tumor necrosis factor-alpha on human
vascular endothelial cells
EM Paleolog, SA Delasalle, WA Buurman and M Feldmann
Kennedy Institute of Rheumatology, Sunley Division, London, UK.
Tumor necrosis factor-alpha (TNF-alpha) plays a critical role in the
control of endothelial cell function and hence in regulating traffic of
circulating cells into tissues in vivo. Stimulation of endothelial cells in
vitro by TNF-alpha increases the surface expression of leukocyte adhesion
molecules, enhances cytokine production, and induces tissue factor
procoagulant activity. In the present study, we have examined the relative
roles of the two cell surface receptors for TNF- alpha (p55 and p75) on
endothelial cells, using antibodies with both agonistic and antagonistic
activities. We report that anti-p55 receptor agonistic antibody Htr-9
induces the expression of tissue factor antigen and the release of
interleukin-8 (IL-8) and granulocyte- macrophage colony-stimulating factor
(GM-CSF). In contrast, there is very little or no activation of endothelial
cell responses by an anti- p75 agonist. TNF-alpha-induced expression of
tissue factor and adhesion molecules, and release of IL-8 and GM-CSF, are
decreased by antibodies with antagonistic activities for either receptor,
although the effect of anti-p55 antibodies is markedly greater than that of
anti-p75 antibodies. The responses of endothelial cells to
lymphotoxin/TNF-beta are significantly decreased by anti-p55 antagonists
alone. Our data suggest that endothelial cell responses to TNF-alpha, such
as expression of tissue factor and adhesion molecules for mononuclear
cells, which may be important in the pathogenesis of atherosclerosis, are
mediated predominantly, but not exclusively, by the p55 TNF receptor.
Volume 84,
Issue 8,
pp. 2578-2590,
10/15/1994
Copyright © 1994 by The American Society of Hematology
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