Involvement of immune mechanisms in the propagation of coagulation in DIC. Interaction of pathogens with neutrophils, macrophages, and platelets induces formation of NETs. Components of NETs, such as histones and DNA/nucleosomes, can further amplify the coagulation pathway leading to thrombin generation. NETs and proinflammatory cytokines promote TF expression on monocytes and TF-mediated coagulation. Cell-free DNA supports contact activation and intrinsic coagulation, whereas extracellular histones activate platelets and induce exocytosis of endothelial storage granules, including WPBs and subsequent release of von Willebrand factor and P-selectin, which promote microvascular thrombosis. Thrombin has a similar secretagogue effect. PSGL-1, P-selectin glycoprotein ligand-1.