Abstract
Deep vein thrombosis (DVT) is a major origin of morbidity and mortality. While DVT has long been considered as blood coagulation disorder, several recent lines of evidence demonstrate that immune cells and inflammatory processes are involved in DVT initiation. Here, we discuss these mechanisms, in particular, the role of immune cells in endothelial activation, and the immune cascades leading to expression of adhesion receptors on endothelial cells. We analyze the specific recruitment and functional roles of different immune cells, such as mast cells and leukocytes, in DVT. Importantly, we also speculate how immune modulation could be used for DVT prevention with a lower risk of bleeding complications than conventional therapeutic approaches.
Highlights
Deep vein thrombosis (DVT) is a major origin of morbidity and mortality
Concluding Remarks Mechanisms of DVT initiation represent a cascade of events virtually identical to the local inflammatory response recently designated as immunothrombosis [99]
This opens a window of opportunities for identification of new antithrombotic targets because (i) the immune system is not directly implicated in normal hemostasis and targeting it is unlikely to result in excessive bleeding; and (ii) multiple anti-inflammatory drugs are already on the market and, available for testing their efficacy to prevent DVT
Summary
While DVT has long been considered as blood coagulation disorder, several recent lines of evidence demonstrate that immune cells and inflammatory processes are involved in DVT initiation. We discuss these mechanisms, in particular, the role of immune cells in endothelial activation, and the immune cascades leading to expression of adhesion receptors on endothelial cells. Activation of FX can occur via two mechanisms designated as extrinsic and intrinsic pathways The former one is initiated by a protein designated as tissue factor (TF), which may be exposed by the tissues or blood cells, predominantly monocytes.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
