ArticleProtein & cell2010
Complement activation by phospholipids: the interplay of factor H and C1q.
Article in Protein & cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 61 citations in OpenAlex.
- Discovery and characterization of vertebrate sialoglycan-binding proteins.Seminars in immunology · 2025Review
- Differential expression of complement Properdin and Factor H in the placentae and umbilical cords of mothers with Preeclampsia, Gestational Diabetes Mellitus and Recurrent Pregnancy Loss.Frontiers in immunology · 2025Article
- New Therapeutic Strategies in Retinal Vascular Diseases: A Lipid Target, Phosphatidylserine, and Annexin A5-A Future Theranostic Pairing in Ophthalmology.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Apoptosis in post-streptococcal glomerulonephritis and mechanisms for failed of inflammation resolution.Pediatric nephrology (Berlin, Germany) · 2024Review
- Reexamining the effects of drug loading on the in vivo performance of PEGylated liposomal doxorubicin.Acta pharmacologica Sinica · 2024Article
- Complement-Coagulation Cross-talk: Factor H-mediated regulation of the Complement Classical Pathway activation by fibrin clots.Frontiers in immunology · 2024Article
- Cutting edge of genetically modified pigs targeting complement activation for xenotransplantation.Frontiers in immunology · 2024Review
- Epigenetic regulation of complement C1Q gene expression.Frontiers in immunology · 2024Article
- Complement Activation-Independent Attenuation of SARS-CoV-2 Infection by C1q and C4b-Binding Protein.Viruses · 2023Article
- Human C1q Regulates Influenza A Virus Infection and Inflammatory Response via Its Globular Domain.International journal of molecular sciences · 2022Article
- Binding of phosphatidylserine-positive microparticles by PBMCs classifies disease severity in COVID-19 patients.Journal of extracellular vesicles · 2021Article
- SARS-CoV-2: Pathogenic Mechanisms and Host Immune Response.Advances in experimental medicine and biology · 2021Article
- Mesenchymal Stem Cells Control Complement C5 Activation by Factor H in Lupus Nephritis.EBioMedicine · 2018Article
- Human C1q Induces Apoptosis in an Ovarian Cancer Cell LineFrontiers in immunology · 2016Article
- Analysis of the Interaction between Globular Head Modules of Human C1q and Its Candidate Receptor gC1qR.Frontiers in immunology · 2016Article
- The endothelial deprotection hypothesis for lupus pathogenesis: the dual role of C1q as a mediator of clearance and regulator of endothelial permeability.F1000Research · 2015Article
- Relative contribution of c1q and apoptotic cell-surface calreticulin to macrophage phagocytosis.Journal of innate immunity · 2014Article
- Identification of a receptor for neuropeptide VGF and its role in neuropathic pain.The Journal of biological chemistry · 2013Article
- Innate immunity and neuroinflammation.Mediators of inflammation · 2013Review
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Complement proteins in blood recognize charged particles. The anionic phospholipid (aPL) cardiolipin binds both complement proteins C1q and factor H. C1q is an activator of the complement classical pathway, while factor H is an inhibitor of the alternative pathway. To examine opposing effects of C1q and factor H on complement activation by aPL, we surveyed C1q and factor H binding, and complement activation by aPL, either coated on microtitre plates or in liposomes. Both C1q and factor H bound to all aPL tested, and competed directly with each other for binding. All the aPL activated the complement classical pathway, but negligibly the alternative pathway, consistent with accepted roles of C1q and factor H. However, in this system, factor H, by competing directly with C1q for binding to aPL, acts as a direct regulator of the complement classical pathway. This regulatory mechanism is distinct from its action on the alternative pathway. Regulation of classical pathway activation by factor H was confirmed by measuring C4 activation by aPL in human sera in which the C1q:factor H molar ratio was adjusted over a wide range. Thus factor H, which is regarded as a down-regulator only of the alternative pathway, has a distinct role in downregulating activation of the classical complement pathway by aPL. A factor H homologue, β2-glycoprotein-1, also strongly inhibits C1q binding to cardiolipin. Recombinant globular domains of C1q A, B and C chains bound aPL similarly to native C1q, confirming that C1q binds aPL via its globular heads.
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Registered trials
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.