ArticlePloS one2016
Identification of a Monoclonal Antibody That Attenuates Antiphospholipid Syndrome-Related Pregnancy Complications and Thrombosis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Understanding the Pathophysiology of Preeclampsia: Exploring the Role of Antiphospholipid Antibodies and Future Directions.Journal of clinical medicine · 2024Review
- Obstetric antiphospholipid syndrome carries an increased lifetime risk for obstetric and thrombotic complications-a population-based study.Research and practice in thrombosis and haemostasis · 2024Article
- Interaction of antiphospholipid antibodies with endothelial cells in antiphospholipid syndrome.Frontiers in immunology · 2024Review
- Role of Lipid Rafts on LRP8 Signaling Triggered by Anti-β2-GPI Antibodies in Endothelial Cells.Biomedicines · 2023Article
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
- Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome.Seminars in immunopathology · 2022Review
- Effects of anti-beta 2-glycoprotein 1 antibodies and its association with pregnancy-related morbidity in antiphospholipid syndrome.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Review
- Protein Phosphatase 2A Activation Via ApoER2 in Trophoblasts Drives Preeclampsia in a Mouse Model of the Antiphospholipid Syndrome.Circulation research · 2021Article
- Catastrophic antiphospholipid syndrome during pregnancy.European journal of obstetrics, gynecology, and reproductive biology · 2021Review
- Targeting Phosphatidylserine Enhances the Anti-tumor Response to Tumor-Directed Radiation Therapy in a Preclinical Model of Melanoma.Cell reports · 2021Article
- NETs in APS: Current Knowledge and Future Perspectives.Current rheumatology reports · 2020Review
- TIMs, TAMs, and PS- antibody targeting: implications for cancer immunotherapy.Cell communication and signaling : CCS · 2020Review
- The role of beta-2-glycoprotein I in health and disease associating structure with function: More than just APS.Blood reviews · 2020Review
- Obstetric Anti-phospholipid Syndrome: State of the Art.Current rheumatology reports · 2018Review
- Article
- Update on Antiphospholipid Syndrome: Ten Topics in 2017.Current rheumatology reports · 2018Review
- Antiphospholipid Antibodies to Domain I of Beta-2-Glycoprotein I Show Different Subclass Predominance in Comparison to Antibodies to Whole Beta-2-glycoprotein I.Frontiers in immunology · 2018Article
- Antibody targeting of phosphatidylserine for detection and immunotherapy of cancer.ImmunoTargets and therapy · 2018Article
- Antiphospholipid syndrome: an update for clinicians and scientists.Current opinion in rheumatology · 2017Review
- Emerging Treatment Models in Rheumatology: Antiphospholipid Syndrome and Pregnancy: Pathogenesis to Translation.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
In the antiphospholipid syndrome (APS), patients produce antiphospholipid antibodies (aPL) that promote thrombosis and adverse pregnancy outcomes. Current therapy with anticoagulation is only partially effective and associated with multiple complications. We previously discovered that aPL recognition of cell surface β2-glycoprotein I (β2-GPI) initiates apolipoprotein E receptor 2 (apoER2)-dependent signaling in endothelial cells and in placental trophoblasts that ultimately promotes thrombosis and fetal loss, respectively. Here we sought to identify a monoclonal antibody (mAb) to β2-GPI that negates aPL-induced processes in cell culture and APS disease endpoints in mice. In a screen measuring endothelial NO synthase (eNOS) activity in cultured endothelial cells, we found that whereas aPL inhibit eNOS, the mAb 1N11 does not, and instead 1N11 prevents aPL action. Coimmunoprecipitation studies revealed that 1N11 decreases pathogenic antibody binding to β2-GPI, and it blocks aPL-induced complex formation between β2-GPI and apoER2. 1N11 also prevents aPL antagonism of endothelial cell migration, and in mice it reverses the impairment in reendothelialization caused by aPL, which underlies the non-thrombotic vascular occlusion provoked by disease-causing antibodies. In addition, aPL inhibition of trophoblast proliferation and migration is negated by 1N11, and the more than 6-fold increase in fetal resorption caused by aPL in pregnant mice is prevented by 1N11. Furthermore, the promotion of thrombosis by aPL is negated by 1N11. Thus, 1N11 has been identified as an mAb that attenuates APS-related pregnancy complications and thrombosis in mice. 1N11 may provide an efficacious, mechanism-based therapy to combat the often devastating conditions suffered by APS patients.
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