Figure 2.
Cooperation between immune cells and factors in VT. In the VT setting, the release of WPBs, the expression of cell adhesion molecules, and inflammasome activation initiate thrombosis. MC degranulation supports VT, at least in part, through MC-derived chymase. The upregulation of podoplanin in the IVC triggers VT through CLEC-2 on platelets. Complement system components C3 and C5 activation supports platelet and neutrophil recruitment. Activated platelets support NETosis through HMGB1-RAGE and P-selectin–PSGL-1 leading to PAD4-dependent release of NETs. NLRP3 activation in neutrophils can be triggered by different mechanisms including SYK and PAD4 axis. NLRP3 activation leads to GDD pore formation and release of IL-1β and IL-18. IL-18 supports NK cell recruitment, release of IFN-γ, and NETosis. Platelet NLRP3 is also activated in VT. NET-associated histones and S100A8/A9 support thrombosis. Hypoxia inside thrombus induces HIF-1α in neutrophils and supports NETosis. AD-1 makes fibrin fibers thicker and protected from fibrinolysis. IL-17 activates ECs and neutrophils and promotes NETosis. Conversely, resolvin D4 prevents thrombus propagation. CAMs, cell adhesion molecules; CLEC-2, C-type lectin like-receptor 2; DPPI, dipeptidyl peptidase I; H3/4, histone H3 and H4. Figure created with BioRender.com.

Cooperation between immune cells and factors in VT. In the VT setting, the release of WPBs, the expression of cell adhesion molecules, and inflammasome activation initiate thrombosis. MC degranulation supports VT, at least in part, through MC-derived chymase. The upregulation of podoplanin in the IVC triggers VT through CLEC-2 on platelets. Complement system components C3 and C5 activation supports platelet and neutrophil recruitment. Activated platelets support NETosis through HMGB1-RAGE and P-selectin–PSGL-1 leading to PAD4-dependent release of NETs. NLRP3 activation in neutrophils can be triggered by different mechanisms including SYK and PAD4 axis. NLRP3 activation leads to GDD pore formation and release of IL-1β and IL-18. IL-18 supports NK cell recruitment, release of IFN-γ, and NETosis. Platelet NLRP3 is also activated in VT. NET-associated histones and S100A8/A9 support thrombosis. Hypoxia inside thrombus induces HIF-1α in neutrophils and supports NETosis. AD-1 makes fibrin fibers thicker and protected from fibrinolysis. IL-17 activates ECs and neutrophils and promotes NETosis. Conversely, resolvin D4 prevents thrombus propagation. CAMs, cell adhesion molecules; CLEC-2, C-type lectin like-receptor 2; DPPI, dipeptidyl peptidase I; H3/4, histone H3 and H4. Figure created with BioRender.com.

This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal