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Contact system sends defensins to the rescue.

In this issue of Blood, Abu-Fanne et al identify a link between activation of the contact system of coagulation involving factor XIIa (FXIIa) and kallikrein, promoting neutrophils to release the antimicrobial peptide α-defensin-1, which enhances fibrin polymerization kinetics, alters fibrin morphology, and inhibits fibrinolysis. These reactions may serve as an extension or consequence of innate immunity and are shown to affect in vivo murine thrombosis.1