The pathogenic mechanisms underlying the increased vascular permeability in dengue hemorrhagic fever (DHF) are not well understood. Enhanced cellular immune activation， especially activation of serotype-cross reactive T cells， has been implicated in plasma leakage in DHF. Changes in several biological markers and mediators including cytokines， chemokines， angiogenic factors and their receptors have been shown to correlate with disease severity. A decline in plasma levels of a soluble form of vascular endothelial growth factor receptor 2 (VEGFR2)， a receptor of vascular endothelial growth factor (VEGF)， has been associated with plasma leakage in dengue patients.
The pathogenic mechanisms underlying the increased vascular permeability in dengue hemorrhagic fever (DHF) are not well understood. Enhanced cellular immune activation， especially activation of serotype-cross reactive T cells， has been implicated in plasma leakage in DHF. Changes in several biological markers and mediators including cytokines， chemokines， angiogenic factors and their receptors have been shown to correlate with disease severity. A decline in plasma levels of a soluble form of vascular endothelial growth factor receptor 2 (VEGFR2)， a receptor of vascular endothelial growth factor (VEGF)， has been associated with plasma leakage in dengue patients.
