Antiphospholipid antibodies activate vascular endothelial cells. Lupus 1996 Oct;5(5):440-1
Date
10/01/1996Pubmed ID
8902777DOI
10.1177/096120339600500521Scopus ID
2-s2.0-0029845565 (requires institutional sign-in at Scopus site) 45 CitationsAbstract
Antiphospholipid antibodies (aPL) are associated with a syndrome of arterial and venous thrombosis and recurrent fetal loss. We have shown that IgG purified from patients with aPL activate vascular endothelial cells (EC), converting the steady-state, non-thrombotic endothelial surface to a pro-thrombotic state. The aPL-activated EC are characterized by the expression of leukocyte adhesion molecules, including ICAM-1, VCAM, and E-selectin. EC activation is dependent upon the presence of beta 2-GP-I, a cofactor necessary for anticardiolipin reactivity. In addition, EC activation is not attributable to endotoxin contamination, Fc receptor interactions, or immune complexes, but rather is the result of the specific anticardiolipin reactivity of the IgG. Endothelial activation by aPL may be an important mechanism by which these antibodies cause a hypercoagulable state.
Author List
Simantov R, Lo SK, Gharavi A, Sammaritano LR, Salmon JE, Silverstein RLAuthor
Roy L. Silverstein MD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Antibodies, AntiphospholipidEndothelium, Vascular
Glycoproteins
Humans
Thrombosis
beta 2-Glycoprotein I
