Properdin (factor P) as a new target cleaved by factor XIa: Intrinsic coagulation at the crossroads with inflammation

Abstract

The complement system and blood coagulation cascade, in particular, the contact activation pathway, are functionally related and exhibit crossover activities. Deficiency or altered function of complement proteins are associated with thrombo‐inflammatory diseases. Factor XI (FXI), as part of the intrinsic pathway, is the zymogen, which can be activated to the plasma protease FXIa by FXIIa with the help of high molecular weight kininogen, and then continue to the downstream cascade of proteases that ultimately triggers the production of thrombin (FIIa).