PMC:7386875 / 10407-12485 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7386875","sourcedb":"PMC","sourceid":"7386875","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7386875","text":"Figure 2. Mechanisms regulating immunothrombosis. In vascular homeostasis, the endothelium possesses anti-inflammatory and antithrombotic properties due to the expression of CD39, nitric oxide (NO), and prostacyclin in addition to the natural anticoagulants, TFPI (tissue factor pathway inhibitor), activated protein C, and thrombomodulin. In the setting of infection or inflammation, endothelial cells upregulate the expression of VWF (von Willebrand factor) and adhesion molecules such as ICAM (intercellular adhesion molecule)-1, αvβ3, P-selectin and E-selectin, promoting the adhesion of leukocytes and platelets. Activated platelets release chemokines CXCL1, PF (platelet factor)-4, CXCL5, CXCL7, CCL3, RANTES (regulated on activation, normal T-cell expressed and secreted), and CCL7 to enhance leukocyte recruitment. Leukocytes interact with platelets via several receptor/ligand pairs. These include platelet P-selectin binding to its cognate receptor PSGL (P-selectin glycoprotein)-1 on leukocytes, GP-Ib on platelets interacting with Mac-1 on monocytes and neutrophils, and GPIIb/IIIa binding to SLC44A2/CTL-2 on neutrophils. Activated platelets release polyphosphate (polyP), which activates the contact pathway, and HMGB (high mobility group box)-1, which enhances monocyte recruitment and monocyte tissue factor (TF) expression, thereby amplifying thrombin generation by way of the TF pathway of coagulation. Neutrophils release neutrophil extracellular traps (NETs) which promote thrombosis via activation of the contact pathway and the binding and activation of platelets. Finally, complement activation leads to the recruitment of leukocytes and upregulates TF expression, amplifies platelet activation and upregulates endothelial expression of proinflammatory cytokines, including IL (interleukin)-1, IL-6, IL-8, and MCP (monocyte chemoattractant protein)-1. These mechanisms result in excess thrombin generation, which potentiates the activation of platelets, leukocytes, and endothelium via PARs (protease-activated receptors) and culminates in a fibrin 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