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Section of Internal Medicine and Oncological Sciences (Center for the Study of Rheumatic Diseases),
Section of Gastroenterology, Department of Clinical and Experimental Medicine, and
Section of Internal and Cardiovascular Medicine, Department of Internal Medicine, University of Perugia, Perugia, Italy; and
European Institute of Oncology, Milan, Italy
Salicylates inhibit T cell adhesion to and transmigration through
endothelium by preventing integrin activation induced by contact with
endothelial cells. In the present study the effects of aspirin and
sodium salicylate on the first steps of T cell adhesion have been
analyzed in a nonstatic in vitro system. Salicylates partially reduced
adhesion to activated endothelium and, in parallel, L-selectin
expression on resting T cells by inducing shedding of the molecule
without affecting its mRNA transcript. The role of L-selectin
down-regulation in reducing T cell adhesion in this system was
supported by the fact that aspirin inhibited T cell adhesion also on
plastic-immobilized L-selectin ligand or when 
4
integrin-mediated adhesion to endothelium was blocked by specific mAbs.
In addition, preincubation of T cells with inhibitors of L-selectin
shedding prevented both functional and phenotypic inhibitory effects of
salicylates. The decrease in T cell adhesion and L-selectin expression
seems to be dependent on intracellular calcium increase and tyrosine
kinase activation, because these effects could be reversed by
preincubating salicylate-treated T cells with EGTA, genistein, or
tyrphostin. Finally, the infusion of aspirin into healthy volunteers
induced down-regulation of L-selectin on circulating T cells. These
results suggest that salicylates interfere not only with integrin
activation, but also with the L-selectin-mediated first steps of T cell
binding to endothelium.
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