|
|
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.
 Previous Article | Next Article 
Submitted April 20, 2006
Accepted August 25, 2006
Current concepts on the pathogenesis of the antiphospholipid syndrome
Bill Giannakopoulos, Freda Passam, Soheila Rahgozar, and Steven A. Krilis*
St. George Hospital, University of New South Wales, Sydney, Australia
Dept of Haematology, St. George Hospital, University of New South Wales, Sydney, Australia
* Corresponding author; email: s.krilis{at}unsw.edu.au.
The antiphospholipid syndrome (APS) is an important cause of acquired thrombophilia. It is characterised 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 ( 2-GPI) and prothrombin. There is an accumulating body of experimental evidence which 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 immunological mechanisms which 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 towards 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:
|
|
|
|
 
B. Giannakopoulos and S. A. Krilis
How I treat the antiphospholipid syndrome
Blood,
September 3, 2009;
114(10):
2020 - 2030.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C Pericleous, I Giles, and A Rahman
Are endothelial microparticles potential markers of vascular dysfunction in the antiphospholipid syndrome?
Lupus,
July 1, 2009;
18(8):
671 - 675.
[Abstract]
[PDF]
|
|
|
|
|
|
|
E. Peerschke, W Yin, D. Alpert, R. Roubey, J. Salmon, and B Ghebrehiwet
Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies
Lupus,
May 1, 2009;
18(6):
530 - 538.
[Abstract]
[PDF]
|
|
|
|
|
|
|
I. Giles, C. Pericleous, X. Liu, J. Ehsanullah, L. Clarke, P. Brogan, M. Newton-West, R. Swerlick, A. Lambrianides, P. Chen, et al.
Thrombin Binding Predicts the Effects of Sequence Changes in a Human Monoclonal Antiphospholipid Antibody on Its In Vivo Biologic Actions
J. Immunol.,
April 15, 2009;
182(8):
4836 - 4843.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y.-H. Yang, D. Chien, M. Wu, J. FitzGerald, J. M. Grossman, B. H. Hahn, K.-K. Hwang, and P. P. Chen
Novel Autoantibodies against the Activated Coagulation Factor IX (FIXa) in the Antiphospholipid Syndrome That Interpose the FIXa Regulation by Antithrombin
J. Immunol.,
February 1, 2009;
182(3):
1674 - 1680.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Y. Chan, F. Andreotti, and R. C. Becker
Hypercoagulable States in Cardiovascular Disease
Circulation,
November 25, 2008;
118(22):
2286 - 2297.
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Avcin, R. Cimaz, E. D. Silverman, R. Cervera, M. Gattorno, S. Garay, Y. Berkun, F. R. Sztajnbok, C. A. Silva, L. M. Campos, et al.
Pediatric Antiphospholipid Syndrome: Clinical and Immunologic Features of 121 Patients in an International Registry
Pediatrics,
November 1, 2008;
122(5):
e1100 - e1107.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R Forastiero and M Martinuzzo
Prothrombotic mechanisms based on the impairment of fibrinolysis in the antiphospholipid syndrome
Lupus,
October 1, 2008;
17(10):
872 - 877.
[Abstract]
[PDF]
|
|
|
|
|
|
|
I Giles, A Lambrianides, and A Rahman
Examining the non-linear relationship between monoclonal antiphospholipid antibody sequence, structure and function
Lupus,
October 1, 2008;
17(10):
895 - 903.
[Abstract]
[PDF]
|
|
|
|
|
|
|
J. Rand, X. Wu, A. Quinn, and D. Taatjes
Resistance to annexin A5 anticoagulant activity: a thrombogenic mechanism for the antiphospholipid syndrome
Lupus,
October 1, 2008;
17(10):
922 - 930.
[Abstract]
[PDF]
|
|
|
|
|
|
|
E Cockrell, R. Espinola, and K. McCrae
Annexin A2: biology and relevance to the antiphospholipid syndrome
Lupus,
October 1, 2008;
17(10):
944 - 952.
[Abstract]
[PDF]
|
|
|
|
|
|
|
R. M. Vanacore, A.-J. L. Ham, J.-P. Cartailler, M. Sundaramoorthy, P. Todd, V. Pedchenko, Y. Sado, D.-B. Borza, and B. G. Hudson
A Role for Collagen IV Cross-links in Conferring Immune Privilege to the Goodpasture Autoantigen: STRUCTURAL BASIS FOR THE CRYPTICITY OF B CELL EPITOPES
J. Biol. Chem.,
August 15, 2008;
283(33):
22737 - 22748.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
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]
|
|
|
|
|
