Signaling by Antiphospholipid (aPL) Antibodies

The antiphospholipid syndrome is characterized by the presence of circulating aPL antibodies, thrombosis, pregnancy loss, preterm birth and increased risk of cardiovascular disease. We have recently discovered that aPL antibodies cause potent antagonism of eNOS activation, which disrupts multiple normal functions of endothelium including the nonadherence of leukocytes. Candidate receptors and adaptor molecules necessary for aPL action have been identified. The ultimate goal is to determine if aPL antibody actions in endothelium can be blocked to prevent the multiple life-threatening manifestations of the antiphospholipid syndrome.


leukocyte adhesion in vivo in mouse microvasculature