ArticleThrombosis and haemostasis2015
Contact activation of C3 enables tethering between activated platelets and polymorphonuclear leukocytes via CD11b/CD18.
Article in Thrombosis and haemostasis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis.The Journal of clinical investigation · 2020Trial
- The role of complement in long COVID pathogenesis.JCI insight · 2025Review
- Cryo-EM analysis of complement C3 reveals a reversible major opening of the macroglobulin ring.Nature structural & molecular biology · 2025Article
- Article
- The Role of Thrombo-inflammation in Ischemic Stroke: Focus on the Manipulation and Clinical Application.Molecular neurobiology · 2025Review
- Costunolide Reduces DN Inflammatory Response and Renal Thrombosis by Inhibiting NET Formation.Journal of diabetes research · 2025Article
- Native C3 is activated without proteolytic cleavage by transformation to C3(HFrontiers in immunology · 2025Article
- Complement: Functions, location and implications.Immunology · 2023Review
- Therapeutic regulation of complement activation in extracorporeal circuits and intravascular treatments with special reference to the alternative pathway amplification loop.Immunological reviews · 2023Review
- Predicting the In Vivo Performance of Cardiovascular Biomaterials: Current Approaches In Vitro Evaluation of Blood-Biomaterial Interactions.International journal of molecular sciences · 2021Review
- Inflammation, Infection and Venous Thromboembolism.Circulation research · 2021Review
- Is complement the culprit behind COVID-19 vaccine-related adverse reactions?The Journal of clinical investigation · 2021Review
- Deficiency of ITGAM Attenuates Experimental Abdominal Aortic Aneurysm in Mice.Journal of the American Heart Association · 2021Article
- The Promiscuous Profile of Complement Receptor 3 in Ligand Binding, Immune Modulation, and Pathophysiology.Frontiers in immunology · 2021Review
- Anti-HLA antibodies with complementary and synergistic interaction geometries promote classical complement activation on platelets.Haematologica · 2019Article
- The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System.Frontiers in immunology · 2019Review
- Complement in Thrombotic Microangiopathies: Unraveling Ariadne's Thread Into the Labyrinth of Complement Therapeutics.Frontiers in immunology · 2019Review
- Properdin: A multifaceted molecule involved in inflammation and diseases.Molecular immunology · 2018Review
- The Complement System in Dialysis: A Forgotten Story?Frontiers in immunology · 2018Review
- Complement component 5 promotes lethal thrombosis.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Complement component C3 has a potential role in thrombotic pathologies. It is transformed, without proteolytic cleavage, into C3(H2O) upon binding to the surface of activated platelets. We hypothesise that C3(H2O) bound to activated platelets and to platelet-derived microparticles (PMPs) contributes to platelet-PMN complex (PPC) formation and to the binding of PMPs to PMNs. PAR-1 activation of platelets in human whole blood from normal individuals induced the formation of CD16+/CD42a+ PPC. The complement inhibitor compstatin and a C5a receptor antagonist inhibited PPC formation by 50 %, while monoclonal antibodies to C3(H2O) or anti-CD11b inhibited PPC formation by 75-100 %. Using plasma protein-depleted blood and blood from a C3-deficient patient, we corroborated the dependence on C3, obtaining similar results after reconstitution with purified C3. By analogy with platelets, PMPs isolated from human serum were found to expose C3(H2O) and bind to PMNs. This interaction was also blocked by the anti-C3(H2O) and anti-CD11b monoclonal antibodies, indicating that C3(H2O) and CD11b are involved in tethering PMPs to PMNs. We confirmed the direct interaction between C3(H2O) and CD11b by quartz crystal microbalance analysis using purified native C3 and recombinant CD11b/CD18 and by flow cytometry using PMP and recombinant CD11b. Transfectants expressing CD11b/CD18 were also shown to specifically adhere to surface-bound C3(H2O). We have identified contact-activated C3(H2O) as a novel ligand for CD11b/CD18 that mediates PPC formation and the binding of PMPs to PMNs. Given the various roles of C3 in thrombotic reactions, this finding is likely to have important pathophysiological implications.
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