title: Molecular pathogenesis of the antiphospholipid syndrome.
abstract: The antiphospholipid (aPL) syndrome is an acquired autoimmune disorder of unknown etiology in which patients present with thrombosis together with laboratory evidence for antibodies in blood that recognize anionic phospholipid-protein complexes. The main antigenic target for the aPL antibodies has been identified to be beta(2) glycoprotein I (beta(2)GPI), a phospholipid-binding protein. The high affinity of aPL antibody-beta(2)GPI complex for phospholipid membranes seems to be a critical step in the mechanism of this disease. This review focuses on some of the major mechanisms that have been proposed to explain this disorder.
authors.affiliation: Thrombosis and Hemostasis Section, Hematology Division, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. jacob.rand@mssm.edu
authors.forename: Jacob H
authors.initials: JH
authors.lastname: Rand
mesh_terms: D000818:Animals; D017304:Annexin A5 / Q000378:metabolism; D017152:Antibodies, Antiphospholipid / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology*; D001779:Blood Coagulation Factors / Q000378:metabolism; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D008954:Models, Biological; D053482:beta 2-Glycoprotein I
chemical_list: D017304:Annexin A5; D017152:Antibodies, Antiphospholipid; D001779:Blood Coagulation Factors; D006023:Glycoproteins; D053482:beta 2-Glycoprotein I