The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Requirement of activation of complement C3 and C5 for antiphospholipid antibody–mediated thrombophilia
Open accessAbstract
Objective: Antiphospholipid antibodies (aPL) have been shown to induce thrombosis, activate endothelial cells, and induce fetal loss. The pathogenesis of aPL‐induced thrombosis, although not completely understood, may involve platelet and endothelial cell activation as well as procoagulant effects of aPL directly on clotting pathway components. Recent studies have shown that uncontrolled complement activation leads to fetal death in aPL‐treated mice. In this study, we tested the hypothesis that aPL are responsible for activation of complement, thus generating split products that induce thrombosis. Methods: To study thrombus dynamics and adhesion of leukocytes we used in vivo murine models of thrombosis and microcirculation, in which injections of aPL were used. Results: Mice deficient in complement components C3 and C5 were resistant to the enhanced thrombosis and endothelial cell activation that was induced by aPL. Furthermore, inhibition of C5 activation using anti‐C5 monoclonal antibodies prevented thrombophilia induced by aPL. Conclusion: These data show that complement activation mediates 2 important effectors of aPL, induction of thrombosis and activation of endothelial cells.
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Cites
A simplification of the protein assay method of Lowry et al. which is more generally applicable
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Complement C3 Activation Is Required for Antiphospholipid Antibody-induced Fetal Loss
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Self-citationComplement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome
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Self-citationComplement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome
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Self-citationMembrane attack by complement: the assembly and biology of terminal complement complexes
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Cited by
Ruiz-Irastorza, G., Crowther, M., Branch, W., & Khamashta, M. A. (2010) · The Lancet · doi:10.1016/s0140-6736(10)60709-x · Cited by 831
The Pathogenesis of the Antiphospholipid Syndrome
Giannakopoulos, B., & Krilis, S. A. (2013) · New England Journal of Medicine · doi:10.1056/nejmra1112830 · Cited by 688
Pathogenesis of antiphospholipid syndrome: understanding the antibodies
Meroni, P. L., Borghi, M. O., Raschi, E., & Tedesco, F. (2011) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2011.52 · Cited by 620
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Antiphospholipid syndrome: advances in diagnosis, pathogenesis, and management
Knight, J. S., Branch, D. W., & Ortel, T. L. (2023) · BMJ · doi:10.1136/bmj-2021-069717 · Cited by 265
Metadata
- Authors
- Pierangeli, S. S., Girardi, G., Vega‐Ostertag, M., Liu, X., Espinola, R. G., & Salmon, J.
- Venue
- Arthritis & Rheumatism
- Publisher
- Wiley
- Published
- 2005-06-28
- Volume
- 52
- Issue
- 7
- Pages
- 2120-2124
- ISSN
- 0004-3591 (ISSN-L)
- 1529-0131
- OpenAlex
- W2008273918
- Cited by
- 362
- References
- 20
- FWCI
- 11.83
- Type
- journal article
- Language
- en
- Open access
- green
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