The FXII-driven contact system. Contact with negatively charged surfaces activates coagulation FXII on endothelial cells, leukocytes, bacteria, and thrombocytes and initiates procoagulant and proinflammatory proteolytic reactions. Activated FXII triggers fibrin formation through the FXI-mediated intrinsic pathway of coagulation. Simultaneously, activation of prekallikrein by FXIIa leads to generation of the vasoactive peptide BK by PK-mediated cleavage of HK.