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Blood, 15 January 2007, Vol. 109, No. 2, pp. 422-430.
Prepublished online as a Blood First Edition Paper on September 19, 2006; DOI 10.1182/blood-2006-04-001206.
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REVIEWS IN TRANSLATIONAL HEMATOLOGY
Current concepts on the pathogenesis of the antiphospholipid syndrome
Bill Giannakopoulos1,
Freda Passam2,
Soheila Rahgozar1, and
Steven A. Krilis1,
1 Department of Immunology, Allergy and Infectious Diseases, Department of Medicine, University of New South Wales, St George Hospital, Kogarah, Sydney, Australia;
2 Department of Haematology, St George Hospital, Kogarah, Sydney, Australia
The antiphospholipid syndrome (APS) is an important cause of acquired thrombophilia. It is characterized by the core clinical manifestations of thrombosis, either venous or arterial, and in women it can also be associated with recurrent fetal loss. The detection of persistently elevated levels of antiphospholipid antibodies (aPL Abs) is a requisite laboratory feature for the diagnosis to be made. The dominant antigenic targets in APS are beta 2-glycoprotein I (ß2-GPI) and prothrombin. There is an accumulating body of experimental evidence that suggests that specific subgroups of aPL Abs may directly contribute to disease pathogenesis. This review critically examines the experimental evidence underlying the various propositions made to explain how these antibodies may predispose to disease in humans. Furthermore, it also examines the evidence relating to the immunologic mechanisms that may contribute to the breakage of peripheral tolerance in this disorder. Delineating the strengths and limitations of the experimental evidence accumulated thus far will hopefully stimulate further experimentation toward achieving the ultimate goal of precisely defining the dominant pathogenic mechanisms operational in APS. This may pave the way for the development of improved therapies.
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