ArticleProceedings of the National Academy of Sciences of the United States of America1999
Prevention of experimental antiphospholipid syndrome and endothelial cell activation by synthetic peptides.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 181 citations in OpenAlex.
- Molecular mimicry in the pathogenesis of autoimmune rheumatic diseases.Journal of translational autoimmunity · 2025Review
- COVID-19 and the antiphospholipid syndrome.Autoimmunity reviews · 2022Review
- Circulating immune-complexes of IgG/IgM bound to B2-glycoprotein-I associated with complement consumption and thrombocytopenia in antiphospholipid syndrome.Frontiers in immunology · 2022Observational
- Dorsolateral medullary infarction during skin infection by Stenotrophomonas maltophilia in a patient with triple antiphospholipid antibody positivity: a case-based review.Clinical rheumatology · 2021Review
- Aneurysms in primary antiphospholipid syndrome: a case-based review.Clinical rheumatology · 2021Review
- Molecular Mechanisms of "Antiphospholipid Antibodies" and Their Paradoxical Role in the Pathogenesis of "Seronegative APS".International journal of molecular sciences · 2020Review
- Article
- Article
- The IgA Isotype of Anti-β2 Glycoprotein I Antibodies Recognizes Epitopes in Domains 3, 4, and 5 That Are Located in a Lateral Zone of the Molecule (L-Shaped).Frontiers in immunology · 2019Article
- Environmental Triggers of Autoreactive Responses: Induction of Antiphospholipid Antibody Formation.Frontiers in immunology · 2019Review
- The microbiome in autoimmune diseases.Clinical and experimental immunology · 2019Review
- Vascular Manifestations in Antiphospholipid Syndrome (APS): Is APS a Thrombophilia or a Vasculopathy?Current rheumatology reports · 2017Review
- Article
- Complement inhibition by hydroxychloroquine prevents placental and fetal brain abnormalities in antiphospholipid syndrome.Journal of autoimmunity · 2016Article
- Immunoreactivity and avidity of IgG anti-β2-glycoprotein I antibodies from patients with autoimmune diseases to different peptide clusters of β2-glycoprotein I.Immunologic research · 2015Article
- The role of the gut microbiota in the pathogenesis of antiphospholipid syndrome.Current rheumatology reports · 2015Review
- Antiphospholipid antibodies attenuate endothelial repair and promote neointima formation in mice.Journal of the American Heart Association · 2014Article
- New tests to detect antiphospholipid antibodies: anti-domain I beta-2-glycoprotein-I antibodies.Current rheumatology reports · 2014Review
- Auto-antibodies as emergent prognostic markers and possible mediators of ischemic cardiovascular diseases.Clinical reviews in allergy & immunology · 2013Review
- The future of autoimmunity.Clinical reviews in allergy & immunology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antiphospholipid syndrome (APS) is characterized by recurrent fetal loss, repeated thromboembolic phenomena, and thrombocytopenia. The syndrome is believed to be caused by antiphospholipid beta-2-glycoprotein-I (beta2GPI)-dependent Abs or anti-beta2GPI Abs by themselves. Using a hexapeptide phage display library, we identified three hexapeptides that react specifically with the anti-beta2GPI mAbs ILA-1, ILA-3, and H-3, which cause endothelial cell activation and induce experimental APS. To enhance the binding of the peptides to the corresponding mAbs, the peptides were lengthened to correspond with the site of the beta2GPI epitope being recognized by these mAbs. As a result, the following three peptides were prepared: A, NTLKTPRVGGC, which binds to ILA-1 mAb; B, KDKATFGCHDGC, which binds to ILA-3 mAb; and C, CATLRVYKGG, which binds to H-3 mAb. Peptides A, B, and C specifically inhibit both in vitro and in vivo the biological functions of the corresponding anti-beta2GPI mAbs. Exposure of endothelial cells to anti-beta2GPI mAbs and their corresponding peptides led to the inhibition of endothelial cell activation, as shown by decreased expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1) and monocyte adhesion. In vivo infusion of each of the anti-beta2GPI mAbs into BALB/c mice, followed by administration of the corresponding specific peptides, prevented the peptide-treated mice from developing experimental APS. The use of synthetic peptides that focus on neutralization of pathogenic anti-beta2GPI Abs represents a possible new therapeutic approach to APS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.