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Neutrophil activation by the tissue factor/Factor VIIa/PAR2 axis mediates fetal death in a mouse model of antiphospholipid syndrome

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Academic year: 2020

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Figure

Figure 1PAR2 is required for aPL-IgG–induced neutrophil activity. (A) Immunohistochemical detection of TF and PAR2 on neutrophils from aPL-IgG– and NH-IgG–treated mice
Figure 2TF/FVIIa/PAR2 signaling is required for aPL-IgG–induced increase in neutrophil activity
Figure 4Simvastatin prevents pregnancy loss in aPL-IgG–treated mice. (
Figure 5Statins inhibit TF and PAR2 synthesis and prevent neutrophil oxidative burst and oxidative damage in aPL-IgG–treated mouse placentas

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