Figure 5 .

Proposed mechanism for the pathogenic effects of aPL antibodies on pregnancy outcome. aPL antibodies are preferentially targeted to the placenta where they may promote platelet and endothelial cell activation and directly induce procoagulant activity through interaction with elements of the coagulation pathway. This activity, however, does not seem to be sufficient to cause fetal loss or growth restriction; C3-/- are protected. Activation of the complement pathway by aPL-IgG overwhelms the normally adequate inhibitory mechanisms and amplifies these effects by stimulating the generation of further potent mediators of effector cell activation, including C3a, C5a, and the C5b-9 MAC. The addition of these complement activation products causes thrombosis, tissue hypoxia, and inflammation within the placenta, and ultimately leads to fetal injury.