Abstract
The complement system comprises a series of proteases and inhibitors that are activated in cascade-like fashion during host defense (Makrides 1998). A growing body of evidence supports the hypothesis that immune mechanisms, including complement activation, are involved in inflammatory conditions associated with vascular injury (Acostan et al. 2004; Giannakopoulos et al. 2007), and disseminated intravascular coagulation associated with massive trauma (Huber-Lang, this volume). We propose that platelets and platelet derived microparticles focus complement to sites of vascular injury where regulated complement activation participates in clearing terminally activated platelets and microparticles from the circulation, and dysregulated complement activation contributes to inflammation and thrombosis. Given the central role of platelets in hemostasis and thrombosis, it is not surprising that activated complement components have been demonstrated in many types of atherosclerotic and thrombotic vascular lesions (Torzewsjki et al. 2007; Niculescu et al. 2004).