Tissue factor is a potent initiator of blood coagulation. In tissue sections, it has been immunologically demonstrated in cells normally not in contact with circulating blood, and elevated activity has been repeatedly demonstrated in peripheral blood monocytes of patients considered to be at risk for thrombosis. Studies with endothelial cells and monocytes in culture have documented the induction of tissue factor synthesis by biochemical mediators of the inflammatory process. Lytic processes, such as those caused by complement activation or viral infections, increase the tissue factor activity several fold over the basal level of the affected cells. Diminished anti-thrombotic properties of endothelium, and induced tissue factor expression in endothelium and monocytes/macrophages, combined with the increased specific procoagulant activity resulting from cell membrane damage, may endow inflammatory foci with dramatically elevated procoagulant activity. Levels of tissue factor activity at which procoagulant mechanisms escape regulation by natural anticoagulant mechanisms and produce thrombosis remain to be determined.