Scientists from the University of Texas Southwestern Medical Center have discovered the mechanism that causes blood clots – also known as thrombosis – in patients with antiphospholipid syndrome (APS).

APS is an autoimmune disease in which bacteria and virus-fighting immune system cells attack healthy body tissues and organs, according to the National Institutes of Health. As a result, abnormal blood clotting occurs.

For this study, the investigators examined the actions of APS antibodies on cultured endothelial cells, which line the inside of blood vessels. The scientists found that blood clot-inducing antibodies recognize a protein called Beta2-Glycoprotein I on the surface of endothelial cells. This surface then interacts with apolipoprotein E receptor (apoER2) – a second protein – which inactivates the production of antithrombotic molecule nitric oxide. In turn, the decrease in nitric oxide initiates thrombosis.

By using mice models, the researchers also found that mice who are genetically predisposed to lack apoER2 can be protected from suffering blood clots when given APS antibodies.

Dr. Chieko Mineo, co-author of the study, said that in addition to these findings, the mechanisms that have been identified which promote thrombosis also occur “in APS during pregnancy to adversely affect the health of both the mother and the fetus.”

The scientists said they are hopeful that this discovery will lead to new therapies to help prevent blood clotting as well as pregnancy complications among APS patients.