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The Role of Complement in the Antiphospholipid Syndrome-Associated Pathology

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Abstract

The antiphospholipid syndrome (APS) is characterized by arterial and/or venous thromboses, pregnancy loss, and the presence of anticardiolipin antibodies. The pathogenic mechanisms that lead to these clinical manifestations are incompletely understood. Although a direct pathogenic role of antiphospholipid antibodies has been established, including their role in endothelial cell and platelet activation, there is growing evidence that activation of the complement pathway may contribute to the pathogenesis of APS. Vital information has been obtained from studies exploring the features of pregnancy morbidity and thrombosis using complement deficient murine models. These studies are providing the foundation for the development of new therapeutic options to optimize the management of APS.

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Authors and Affiliations

  1. Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis St, Suite 4B, Boston, MA, 02215, USA

    Ingrid Avalos & George C. Tsokos

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  1. Ingrid Avalos
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  2. George C. Tsokos
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Correspondence to Ingrid Avalos.

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Sources of Funding

ACR/REF Lupus Investigator Fellowship Award and W81XWH-07-1-0286 from Medical Research and Materiel Command.

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Avalos, I., Tsokos, G.C. The Role of Complement in the Antiphospholipid Syndrome-Associated Pathology. Clinic Rev Allerg Immunol 36, 141–144 (2009). https://doi.org/10.1007/s12016-008-8109-7

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  • DOI: https://doi.org/10.1007/s12016-008-8109-7

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