Complement C3 Activation Is Required for Antiphospholipid Antibody-induced Fetal Loss

Complement C3 Activation Is Required for Antiphospholipid Antibody-induced Fetal Loss

The antiphospholipid syndrome (APS) is characterized by recurrent fetal loss, vascular thrombosis, and thrombocytopenia occurring in the presence of antiphospholipid (aPL) antibodies. The pathogenesis of fetal loss and tissue injury in APS is incompletely understood, but is thought to involve platelet and endothelial cell activation as well as procoagulant effects of aPL antibodies acting direc...

Complement activation as a mediator of antiphospholipid antibody induced pregnancy loss and thrombosis.

The antiphospholipid antibody syndrome (APS) is characterised by increased risk of vascular thrombosis involving venous, arterial, and placental circulations. The last of these is associated with poor obstetrical outcomes, including fetal death and growth retardation. Pregnancy loss is a defining criterion for APS and occurs with particularly high frequency in systemic lupus erythematosus (SLE)...

A Case of Gaucher\'s Disease with Recurrent Fetal Loss and Antiphospholipid Antibody Syndrome

The preventative role of heparin in antiphospholipid antibody-induced fetal loss

Tissue factor: a link between C5a and neutrophil activation in antiphospholipid antibody induced fetal injury.

Fetal loss in patients with antiphospholipid (aPL) antibodies has been ascribed to thrombosis of placental vessels. However, we have shown that inflammation, specifically activation of complement with generation of the anaphylotoxin C5a, is an essential trigger of fetal injury. In this study, we analyzed the role of the procoagulant molecule tissue factor (TF) in a mouse model of aPL antibody-i...