ArticleMolecular immunology2019
Complement activation on neutrophils initiates endothelial adhesion and extravasation.
Article in Molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
19 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Recent research progress and future directions of intracerebral hemorrhage.Frontiers in immunology · 2026Review
- Complement system in tumor growth and metastases.British journal of cancer · 2026Review
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Extracellular traps in peripheral blood mononuclear cell fraction in childhood-onset systemic lupus erythematosus.Scientific reports · 2024Article
- The Role of the Complement System in Synaptic Pruning after Stroke.Aging and disease · 2024Review
- Endothelial cell sphingosine 1-phosphate receptor 1 restrains VE-cadherin cleavage and attenuates experimental inflammatory arthritis.JCI insight · 2024Article
- Neutrophils in the periodontium: Interactions with pathogens and roles in tissue homeostasis and inflammation.Immunological reviews · 2023Review
- Neutrophil-activating therapy for the treatment of cancer.Cancer cell · 2023Article
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
- Activation of C3 and C5 May Be Involved in the Inflammatory Progression of PCM and GM.Inflammation · 2022Article
- Natural cell based biomimetic cellular transformers for targeted therapy of digestive system cancer.Theranostics · 2022Review
- Role of complement C1q/C3-CR3 signaling in brain injury after experimental intracerebral hemorrhage and the effect of minocycline treatment.Frontiers in immunology · 2022Article
- Anaphylatoxins orchestrate Th17 response via interactions between CD16+ monocytes and pleural mesothelial cells in tuberculous pleural effusion.PLoS neglected tropical diseases · 2021Article
- Coronavirus infection: An immunologists' perspective.Scandinavian journal of immunology · 2021Review
- The role of complement in brain injury following intracerebral hemorrhage: A review.Experimental neurology · 2021Review
- Proteomic, biomechanical and functional analyses define neutrophil heterogeneity in systemic lupus erythematosus.Annals of the rheumatic diseases · 2021Article
- Modeling the Early Steps of Ovarian Cancer Dissemination in an Organotypic Culture of the Human Peritoneal Cavity.Advances in experimental medicine and biology · 2021Review
- Neutrophil interactions with the sexually transmitted parasiteOpen biology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophils are essential to the pathogenesis of many inflammatory diseases. In the autoantibody-mediated K/BxN model of inflammatory arthritis, the alternative pathway (AP) of complement and Fc gamma receptors (FcγRs) are required for disease development while the classical pathway is dispensable. The reason for this differential requirement is unknown. We show that within minutes of K/BxN serum injection complement activation (CA) is detected on circulating neutrophils, as evidenced by cell surface C3 fragment deposition. CA requires the AP factor B and FcγRs but not C4, implying that engagement of FcγRs by autoantibody or immune complexes directly triggers AP C3 convertase assembly. The absence of C5 does not prevent CA on neutrophils but diminishes the upregulation of adhesion molecules. In vivo two-photon microscopy reveals that CA on neutrophils is critical for neutrophil extravasation and generation of C5a at the site of inflammation. C5a stimulates the release of neutrophil proteases, which contribute to the degradation of VE-cadherin, an adherens junction protein that regulates endothelial barrier integrity. C5a receptor antagonism blocks the extracellular release of neutrophil proteases, suppressing VE-cadherin degradation and neutrophil transendothelial migration in vivo. These results elucidate the AP-dependent intravascular neutrophil-endothelial interactions that initiate the inflammatory cascade in this disease model but may be generalizable to neutrophil extravasation in other inflammatory processes.
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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.