Contact system revisited: an interface between inflammation, coagulation, and innate immunity

A T Long; E Kenne; R Jung; T A Fuchs; T Renné

doi:10.1111/jth.13235

Contact system revisited: an interface between inflammation, coagulation, and innate immunity

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Contact system revisited: an interface between inflammation, coagulation, and innate immunity. / Long, A T; Kenne, E; Jung, R; Fuchs, T A; Renné, T.

In: J THROMB HAEMOST, Vol. 14, No. 3, 03.2016, p. 427-37.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Long, AT, Kenne, E, Jung, R, Fuchs, TA & Renné, T 2016, 'Contact system revisited: an interface between inflammation, coagulation, and innate immunity', J THROMB HAEMOST, vol. 14, no. 3, pp. 427-37. https://doi.org/10.1111/jth.13235

APA

Long, A. T., Kenne, E., Jung, R., Fuchs, T. A., & Renné, T. (2016). Contact system revisited: an interface between inflammation, coagulation, and innate immunity. J THROMB HAEMOST, 14(3), 427-37. https://doi.org/10.1111/jth.13235

Vancouver

Long AT, Kenne E, Jung R, Fuchs TA, Renné T. Contact system revisited: an interface between inflammation, coagulation, and innate immunity. J THROMB HAEMOST. 2016 Mar;14(3):427-37. https://doi.org/10.1111/jth.13235

Bibtex

@article{e7c17a51994b42bfa3492d3c78dad704,

title = "Contact system revisited: an interface between inflammation, coagulation, and innate immunity",

abstract = "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.",

author = "Long, {A T} and E Kenne and R Jung and Fuchs, {T A} and T Renn{\'e}",

note = "{\textcopyright} 2015 International Society on Thrombosis and Haemostasis.",

year = "2016",

month = mar,

doi = "10.1111/jth.13235",

language = "English",

volume = "14",

pages = "427--37",

journal = "J THROMB HAEMOST",

issn = "1538-7933",

publisher = "Wiley-Blackwell",

number = "3",

}

RIS

TY - JOUR

T1 - Contact system revisited: an interface between inflammation, coagulation, and innate immunity

AU - Long, A T

AU - Kenne, E

AU - Jung, R

AU - Fuchs, T A

AU - Renné, T

PY - 2016/3

Y1 - 2016/3

N2 - 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.

AB - 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.

U2 - 10.1111/jth.13235

DO - 10.1111/jth.13235

M3 - SCORING: Journal article

C2 - 26707513

VL - 14

SP - 427

EP - 437

JO - J THROMB HAEMOST

JF - J THROMB HAEMOST

SN - 1538-7933

IS - 3

ER -