Thrombosis as an intravascular effector of innate immunity
By B. Engelmann, Steffen Massberg. Nature reviews. Immunology, 2012
1,769 citations recorded by the source corpus.
Subfields: Hematology, Internal Medicine
View Paper: https://www.semanticscholar.org/paper/17f43a2c8c79ec0e3f9f7ffe446414b9e42a1570
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Milka Koupenova
- K. Martinod
- D. Wagner
- L. Clancy
- L. Acquasaliente
- Heather A. Corkrey
- J. Freedman
- V. De Filippis
Citations in the corpus
- Thrombosis: tangled up in NETs. (2014, background): “Fibrin and NETs likely work together toward immune defense in a process now defined as immunothrombosis.(45) NET fibers contain various other factors that can render them procoagulant.”
- Intelligent Image-Activated Cell Sorting. (2018, neutral): “Recent findings suggest that immunothrombosis, initiated by the innate immune system, consists of neutrophils, monocytes, and platelets and contributes to arterial and/or venous thrombosis (Engelmann and Massberg, 2013).”
- Cytokine Storms: Understanding COVID-19 (2020, neutral): “This process, termed immuno-thrombosis (Engelmann and Massberg, 2013), can also amplify the production of cytokines and is exemplified by links of thrombin with inflammasome activation and production of IL-1.”
- Circulating Platelets as Mediators of Immunity, Inflammation and Thrombosis (2018, background): “” During this process, platelets and immune cells form a physical barrier of confinement preventing dissemination of pathogens and potentially leading to the activation of the innate and adaptive branches of the immune system.(6,9) Interestingly, platelets mediate the crosstalk between the hemostati”
- Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis (2020, background): “pathways, deregulated inflammation, thrombosis and endothelial dysfunction (2, 4).”
- Non-canonical proteolytic activation of human prothrombin by subtilisin from Bacillus subtilis may shift the procoagulant–anticoagulant equilibrium toward thrombosis (2017, background): “Very recently, fibrin generation has been proposed as a host defense mechanism of innate immunity to avoid systemic activation of coagulation by segregating bacterial pathogens in a fibrin network at infection sites (66).”