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Contact system revisited: an interface between inflammation, coagulation, and innate immunity
Author(s) -
Long A. T.,
Kenne E.,
Jung R.,
Fuchs T. A.,
Renné T.
Publication year - 2016
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/jth.13235
Subject(s) - factor xii , coagulation , zymogen , proinflammatory cytokine , innate immune system , inflammation , microbiology and biotechnology , kallikrein , chemistry , thrombus , contact system , immunology , prekallikrein , platelet , complement system , biology , medicine , immune system , biochemistry , enzyme , mechanical engineering , engineering
Summary The contact system is a plasma protease cascade initiated by factor XII (FXII) that activates the proinflammatory kallikrein‐kinin system and the procoagulant intrinsic coagulation pathway. Anionic surfaces induce FXII zymogen activation to form proteolytically active FXIIa. Bacterial surfaces also have the ability to activate contact system proteins, indicating an important role for host defense using the cooperation of the inflammatory and coagulation pathways. Recent research has shown that inorganic polyphosphate found in platelets activates FXII in vivo and can induce coagulation in pathological thrombus formation. Experimental studies have shown that interference with FXII provides thromboprotection without a therapy‐associated increase in bleeding, renewing interest in the FXIIa‐driven intrinsic pathway of coagulation as a therapeutic target. This review summarizes how the contact system acts as the cross‐road of inflammation, coagulation, and innate immunity.