ArticleBlood2011
β₂-Glycoprotein-1 autoantibodies from patients with antiphospholipid syndrome are sufficient to potentiate arterial thrombus formation in a mouse model.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- A systematic review of the association between anti-β-2 glycoprotein I antibodies and APS manifestations.Blood advances · 2021Pooled it
- Deciphering Platelet Transcriptomic Profiles in Antiphospholipid Syndrome: Insights into Their Role as Immunological Players.International journal of molecular sciences · 2026Article
- In vivo targeting of open prothrombin with the monoclonal antibody POmAb results in anticoagulation without excessive bleeding.Journal of thrombosis and haemostasis : JTH · 2026Article
- Animal models of antiphospholipid syndrome.Frontiers in immunology · 2026Review
- The role of neutrophil extracellular traps in antiphospholipid syndrome.Frontiers in immunology · 2026Review
- Mechanism of antiphospholipid antibody-mediated thrombosis in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- A proteomic map of thromboinflammatory signatures in antiphospholipid syndrome: results from antiphospholipid syndrome alliance for clinical trials and international networking (APS ACTION) registry.Frontiers in immunology · 2025Article
- Novel advances on pathophysiological mechanisms, clinical manifestations, and treatment of antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Defective germinal center selection results in persistence of self-reactive B cells from the primary to the secondary repertoire in Primary Antiphospholipid Syndrome.Nature communications · 2024Article
- Advances in the Pathophysiology of Thrombosis in Antiphospholipid Syndrome: Molecular Mechanisms and Signaling through Lipid Rafts.Journal of clinical medicine · 2023Review
- Article
- Cerebral Vein Thrombosis in the Antiphospholipid Syndrome: Analysis of a Series of 27 Patients and Review of the Literature.Brain sciences · 2021Article
- VWF, Platelets and the Antiphospholipid Syndrome.International journal of molecular sciences · 2021Review
- Understanding the Pathophysiology of Thrombotic APS through Animal Models.International journal of molecular sciences · 2021Review
- The J-elongated conformation of βThe Journal of biological chemistry · 2020Article
- Complement activity and complement regulatory gene mutations are associated with thrombosis in APS and CAPS.Blood · 2020Article
- Tissue factor pathway inhibitor primes monocytes for antiphospholipid antibody-induced thrombosis.Blood · 2019Article
- Low extracellular vesicle-associated tissue factor activity in patients with persistent lupus anticoagulant and a history of thrombosis.Annals of hematology · 2019Article
- Complement in the Pathophysiology of the Antiphospholipid Syndrome.Frontiers in immunology · 2019Review
- Renal involvement in antiphospholipid syndrome.Rheumatology international · 2018Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Antiphospholipid syndrome is characterized by thrombosis, recurrent fetal loss, and the presence of the lupus anticoagulant, anticardiolipin antibodies, or anti-β(2)-glycoprotein-1 (anti-β(2)-GP1) antibodies. Although anti-β(2)-GP1 antibodies have been documented as a biomarker for diagnosis of antiphospholipid syndrome, their direct role in the pathogenesis of thrombosis is unknown. We have demonstrated using intravital microscopy that anti-β(2)-GP1 autoantibodies purified from the sera of patients with antiphospholipid syndrome complicated by thrombosis greatly amplify thrombus size after laser-induced vessel wall injury in live mice. Anti-β(2)-GP1 autoantibodies from 3 patients with antiphospholipid syndrome were affinity-purified using human β(2)-GP1 bound to agarose. The effects of purified anti-β(2)-GP1 IgG autoantibodies, of anti-β(2)-GP1-depleted IgG, and of IgG from normal human sera on thrombus formation were measured in mice after arterial injury in the cremaster muscle. Before injury, purified anti-β(2)-GP1 IgG autoantibodies, anti-β(2)-GP1 antibody-depleted IgG, or IgG from normal human sera were infused. Increasing amounts of purified anti-β(2)-GP1 autoantibodies increased thrombus size in a dose-dependent manner, whereas neither anti-β(2)-GP1 antibody-depleted IgG nor IgG from normal serum affected thrombus size. These results indicate that anti-β(2)-GP1 IgG autoantibodies in antiphospholipid syndrome patient sera are not only a marker of antiphospholipid syndrome but are directly involved in the pathogenesis of thrombosis.
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