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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. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-001206v1 109/2/422    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Giannakopoulos, B. Articles by Krilis, S. A. Search for Related Content PubMed PubMed Citation Articles by Giannakopoulos, B. Articles by Krilis, S. A. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Reviews in Translational Hematology Review Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Shoenfeld, P. L. Meroni, and R. Cervera Antiphospholipid syndrome dilemmas still to be solved: 2008 status Ann Rheum Dis, April 1, 2008; 67(4): 438 - 442. [Full Text] [PDF] A. Membre, D. Wahl, V. Latger-Cannard, J.-P. Max, P. Lacolley, T. Lecompte, and V. Regnault The effect of platelet activation on the hypercoagulability induced by murine monoclonal antiphospholipid antibodies Haematologica, April 1, 2008; 93(4): 566 - 573. [Abstract] [Full Text] [PDF] K. R. McCrae Tissue factor needs a "complement" Blood, October 1, 2007; 110(7): 2228 - 2228. [Full Text] [PDF] J. H. Rand The Antiphospholipid Syndrome Hematology, January 1, 2007; 2007(1): 136 - 142. [Abstract] [Full Text] [PDF]

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