ArticleJournal of thrombosis and haemostasis : JTH2021
Anti-β2-glycoprotein I and anti-prothrombin antibodies cause lupus anticoagulant through different mechanisms of action.
Article in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Pooled it
- Cross-Reactivity of Antiphospholipid Antibodies with Gut Commensal Proteins in Antiphospholipid Syndrome.TH open : companion journal to thrombosis and haemostasis · 2026Article
- Antiphospholipid Syndrome: An Antibody-Mediated Disease With Emerging Therapeutic Opportunities.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- The role of activated partial thromboplastin time-clot waveform analysis in distinguishing positive samples of lupus anticoagulant from hemophilia A.Journal of thrombosis and thrombolysis · 2025Article
- Lupus anticoagulant and antiprothrombin antibodies: embracing the future.Journal of thrombosis and haemostasis : JTH · 2025Review
- Review
- Antiphospholipid antibodies induce endothelial procoagulant activity and release of extracellular vesicles independently of a second hit.Frontiers in immunology · 2025Article
- Problem Solved? An Individual Ratio between Point-of-Care and Venous International Normalized Ratio Values in Two Patients with Antiphospholipid Syndrome: Two Case Reports.TH open : companion journal to thrombosis and haemostasis · 2025Article
- Interference of lupus anticoagulant causing antiprothrombin and anti-beta-2-glycoprotein I antibodies on international normalized ratio measurements: comparative analysis of international normalized ratio methods.Research and practice in thrombosis and haemostasis · 2024Article
- Review
- Article
- Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.Blood · 2024Article
- Criteria and Non-Criteria Antiphospholipid Antibodies in Antiphospholipid Syndrome: How Strong Are They Correlated?Biomedicines · 2023Article
- Interference in point-of-care international normalized ratio monitoring in patients with lupus anticoagulant is correlated with anti-β2-glycoprotein I antibody titers.Research and practice in thrombosis and haemostasis · 2023Article
- Dysregulated haemostasis in thrombo-inflammatory disease.Clinical science (London, England : 1979) · 2022Review
- Pathophysiology of Antiphospholipid Syndrome.Thrombosis and haemostasis · 2022Article
- Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins.PLoS pathogens · 2021Article
- Pathogenic lipid-binding antiphospholipid antibodies are associated with severity of COVID-19.Journal of thrombosis and haemostasis : JTH · 2021Article
- Anticardiolipin and other antiphospholipid antibodies in critically ill COVID-19 positive and negative patients.Annals of the rheumatic diseases · 2021Article
- Antiphospholipid Antibody Assays in 2021: Looking for a Predictive Value in Addition to a Diagnostic One.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe presence of lupus anticoagulant (LA) is an independent risk factor for thrombosis. This laboratory phenomenon is detected as a phospholipid-dependent prolongation of the clotting time and is caused by autoantibodies against beta2-glycoprotein I (β2GPI) or prothrombin. How these autoantibodies cause LA is unclear.
objectiveTo elucidate how anti-β2GPI and anti-prothrombin antibodies cause the LA phenomenon.
methodsThe effects of monoclonal anti-β2GPI and anti-prothrombin antibodies on coagulation were analyzed in plasma and with purified coagulation factors.
resultsDetection of LA caused by anti-β2GPI or anti-prothrombin antibodies required the presence of the procofactor factor V (FV) in plasma. LA effect disappeared when FV was replaced by activated FV (FVa), both in a model system and in patient plasma, although differences between anti-β2GPI and anti-prothrombin antibodies were observed. Further exploration of the effects of the antibodies on coagulation showed that the anti-β2GPI antibody attenuated FV activation by activated faxtor X (FXa), whereas the anti-prothrombin antibody did not. Binding studies showed that β2GPI--antibody complexes directly interacted with FV with high affinity. Anti-prothrombin complexes caused the LA phenomenon through competition for phospholipid binding sites with coagulation factors as reduced FXa binding to lipospheres was observed with flow cytometry in the presence of these antibodies.
conclusionAnti-β2GPI and anti-prothrombin antibodies cause LA through different mechanisms of action: While anti-β2GPI antibodies interfere with FV activation by FXa through a direct interaction with FV, anti-prothrombin antibodies compete with FXa for phospholipid binding sites. These data provide leads for understanding the paradoxical association between thrombosis and a prolonged clotting time in the antiphospholipid syndrome.
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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.