Acute coronary diseases are characterized by elevated levels of circulating platelet-leukocyte complexes, raising the possibility that proinflammatory processes might be initiated in leukocytes after platelet adhesion. Here we examined the mechanism of platelet binding to polymorphonuclear leukocytes, monocytes, and monocyte subsets and investigated the potential functional consequences of monocyte binding to minimally activated or thrombin-activated platelets.
|Number of pages||8|
|Journal||Arteriosclerosis, Thrombosis, and Vascular Biology|
|Publication status||Published - Aug 2008|