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CD40L stabilizes arterial thrombi by a β3 integrin–dependent mechanism
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CD40L stabilizes arterial thrombi by a β3 integrin–dependent mechanism
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Journal Article
CD40L stabilizes arterial thrombi by a β3 integrin–dependent mechanism
2002
Overview
CD40L, a member of the tumor necrosis factor family of ligands, plays a major role in immune responses via its receptor, CD40. Recently, CD40L has been detected on the surfaces of activated platelets and shown to activate endothelium. Here we further addressed the function of platelet CD40L. We show that absence of CD40L affects the stability of arterial thrombi and delays arterial occlusion
in vivo
. Infusion of recombinant soluble (rs)CD40L restored normal thrombosis, whereas rsCD40L lacking the KGD integrin-recognition sequence did not. CD40-deficient mice exhibited normal thrombogenesis. rsCD40L specifically bound to purified integrin α
IIb
β
3
and to activated platelets in a β
3
-dependent manner and induced platelet spreading. In addition, rsCD40L promoted the aggregation of either human or mouse platelets under high shear rates. Thus, CD40L appears to be an α
IIb
β
3
ligand, a platelet agonist, and necessary for stability of arterial thrombi.
Publisher
Nature Publishing Group US,Nature Publishing Group
