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Proposed hypothetical model for elevated TAFI and its role in the pathogenesis of NPs. In NPs, down regulation of tPA and elevated FXIIIA enhance fibrin formation in the presence of a Th2 milieu. Inflammatory cells produce inflammatory mediators that lead to vascular leakage, which also increases TAFI levels in NPs. In addition, thrombin (TATc) activates TAFI, which contributes to the down regulation of fibrinolysis further by attenuating the fibrinolysis cascade.
