ArticleThe Journal of biological chemistry2010
Annexin-II, DNA, and histones serve as factor H ligands on the surface of apoptotic cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 78 citations in OpenAlex.
- Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton.Communications biology · 2026Article
- Complement activation in anti-glomerular basement membrane disease before and after treatment with imlifidase.Clinical kidney journal · 2026Article
- Analysis of human factor H-related gene and protein expressed in rheumatoid arthritis synovium identifies a novel mechanism promoting dysregulated complement pathway activation.Scientific reports · 2025Article
- Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 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
- The Complement System as a Part of Immunometabolic Post-Exercise Response in Adipose and Muscle Tissue.International journal of molecular sciences · 2024Review
- Protective role of complement factor H against the development of preeclampsia.Frontiers in immunology · 2024Article
- Voluntary wheel running prevents formation of membrane attack complexes and myelin degradation after peripheral nerve injury.Brain, behavior, and immunity · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Cell-autonomous regulation of complement C3 by factor H limits macrophage efferocytosis and exacerbates atherosclerosis.Immunity · 2023Article
- The Factor H protein family: The switchers of the complement alternative pathway.Immunological reviews · 2023Review
- A disturbed balance between blood complement protective factors (FH, ApoE) and common pathway effectors (C5a, TCC) in acute COVID-19 and during convalesce.Scientific reports · 2022Article
- Article
- Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022Article
- Article
- Associations between the Complement System and Choroidal Neovascularization in Wet Age-Related Macular Degeneration.International journal of molecular sciences · 2020Review
- Skeletal muscle proteome of piglets is affected in a muscle-dependent manner by a limiting total sulfur amino acid supply.European journal of nutrition · 2020Article
- A genome-wide association study identifies key modulators of complement factor H binding to malondialdehyde-epitopes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Interaction of the Factor H Family Proteins FHR-1 and FHR-5 With DNA and Dead Cells: Implications for the Regulation of Complement Activation and Opsonization.Frontiers in immunology · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Apoptotic cells are opsonized by complement components such as C1q and C3b, which increases their susceptibility to phagocytosis. Soluble complement inhibitors such as factor H (fH) also recognize apoptotic cells to minimize the pro-inflammatory effects of downstream complement activation. We used four radiolabeled protein constructs that span different regions of the 20 complement control protein (CCP) modules that make up fH and found that fragments comprising CCPs 6-8, CCPs 8-15, and CCPs 19-20 but not CCPs 1-4, bound to apoptotic Jurkat T cells. There are four possible ligand types on apoptotic cells that could recruit fH: proteins, carbohydrates, lipids, and DNA. We found that CCPs 6-8 of fH bind to annexin-II, a trypsin-insensitive protein that becomes exposed on surfaces of apoptotic cells. The second ligand of fH, which interacts with CCPs 6-8 and 19-20, is DNA. Confocal microscopy showed co-localization of fH with antibodies specific for DNA. fH also binds to histones devoid of DNA, and CCPs 1-4, 6-8, and 8-15 mediate this interaction. Treatment of apoptotic cells with neuraminidase, chondroitinase, heparitinase, and heparinase did not change fH binding. Treatment of apoptotic cells with phospholipase A(2) dramatically increased both binding of fH and cell-surface DNA. We also excluded the possibility that fH interacts with lysophospholipids using surface plasmon resonance and flow cytometry with lipid-coated beads. Identification of annexin-II as one of the fH ligands on apoptotic cells together with the fact that autoantibodies against annexin-II are found in systemic lupus erythematosus provides further insight into understanding the pathogenesis of this disease.
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