Induction of cellular procoagulant activity by the membrane attack complex of complement.

In addition to their well-recognized role in immune defense, there is a growing recognition that the proteins of the complement system impact directly on vascular homeostatic mechanisms, evoking cellular responses that serve to both promote adherence of blood cells to the walls of blood vessels, and the formation of fibrin through the enzyme mechanisms of the coagulation system. This clot-promoting or 'procoagulant' activity initiated through the complement system entails both receptor-mediated as well as receptor-independent pathways of cell activation. In this review, we will focus specifically upon the role that is now thought to be played by the membrane attack complex of the complement system (MAC) in the induction of the procoagulant properties of human platelets and endothelium.