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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4375-4382.
Prepublished online as a Blood First Edition Paper on February 21, 2006; DOI 10.1182/blood-2005-07-2636.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Autoantibodies against the fibrinolytic receptor, annexin 2, in antiphospholipid syndrome
Gabriela Cesarman-Maus,
Nina P. Ríos-Luna,
Arunkumar B. Deora,
Bihui Huang,
Rosario Villa,
Maria del Carmen Cravioto,
Donato Alarcón-Segovia,
Jorge Sánchez-Guerrero, and
Katherine A. Hajjar
From the Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY; and the Departments of Hematology, Immunology and Rheumatology, and Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (INCMNSZ), Mexico City, Mexico.
The association of thrombosis and gestational morbidity with antiphospholipid antibodies is termed antiphospholipid syndrome (APS). Annexin 2 (A2) is a profibrinolytic endothelial cell surface receptor that binds plasminogen, its tissue activator (tPA), and  2-glycoprotein I (2GPI), the main antigen for antiphospholipid antibodies. Here, we evaluate A2 as a target antigen in APS. Serum samples from 434 individuals (206 patients with systemic lupus erythematosus without thrombosis, 62 with APS, 21 with nonautoimmune thrombosis, and 145 healthy individuals) were analyzed by enzyme-linked immunosorbent assay (ELISA) and immunoblot for antiphospholipid and A2 antibodies. Anti-A2 antibodies (titer > 3 SDs) were significantly more prevalent in patients with APS (22.6%; venous, 17.5%; arterial, 34.3%; and mixed thrombosis, 40.4%) than in healthy individuals (2.1%, P < .001), patients with nonautoimmune thrombosis (0%, P = .017), or patients with lupus without thrombosis (6.3%, P < .001). Anti–A2 IgG enhanced the expression of tissue factor on endothelial cells (6.4-fold ± 0.13-fold SE), blocked A2-supported plasmin generation in a tPAdependent generation assay (19%-71%) independently of 2GPI, and inhibited cell surface plasmin generation on human umbilical vein endothelial cells (HUVECs) by 34% to 83%. We propose that anti-A2 antibodies contribute to the prothrombotic diathesis in antiphospholipid syndrome.
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