ArticleThe Journal of clinical investigation2020
Complement activation on endothelium initiates antibody-mediated acute lung injury.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
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
41 citing papers in PubMed, 55 citations in OpenAlex.
- Transfusion-related Acute Lung Injury: 36 Years of Progress (1985-2021).Annals of the American Thoracic Society · 2022Trial
- Airway molecular signatures in antibody-mediated lung transplant rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Review
- Alloantibody IgG subclasses have differential activity in clearing transfused platelets in mice.Blood advances · 2026Article
- Pulmonary Microvascular Endothelial Antigen Presentation Activates resident CD8Research square · 2026Article
- Mouse Models of Transfusion-Related Acute Lung Injury (TRALI).Methods in molecular biology (Clifton, N.J.) · 2026Article
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Bone Marrow Mesenchymal Stem Cell-Derived Exosomes Promote M2 Polarization and Protect Against Acute Lung Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids.Cell reports. Medicine · 2025Article
- tRF-5004b Enriched Secretory Autophagosomes Induce Endothelial Cell Activation to Drive Acute Respiratory Distress Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Intravital imaging of pulmonary lymphatics in inflammation and metastatic cancer.The Journal of experimental medicine · 2025Article
- Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Activation of platelets and the complement system in mice withAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Intravital imaging of pulmonary lymphatics in inflammation and metastatic cancer.bioRxiv : the preprint server for biology · 2024Article
- Complement-Mediated Two-Step NETosis: Serum-Induced Complement Activation and Calcium Influx Generate NADPH Oxidase-Dependent NETs in Serum-Free Conditions.International journal of molecular sciences · 2024Article
- CD94The European respiratory journal · 2024Article
- Reply: The importance of disrupting complement activation in acute lung injury.The Journal of clinical investigation · 2024Article
- Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.The Journal of clinical investigation · 2024Article
- Loss of neutrophil Shp1 produces hemorrhagic and lethal acute lung injury.bioRxiv : the preprint server for biology · 2024Article
- IgG hexamers initiate acute lung injury.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Antibodies targeting human leukocyte antigen (HLA)/major histocompatibility complex (MHC) proteins limit successful transplantation and transfusion, and their presence in blood products can cause lethal transfusion-related acute lung injury (TRALI). It is unclear which cell types are bound by these anti-leukocyte antibodies to initiate an immunologic cascade resulting in lung injury. We therefore conditionally removed MHC class I (MHC I) from likely cellular targets in antibody-mediated lung injury. Only the removal of endothelial MHC I reduced lung injury and mortality, related mechanistically to absent endothelial complement fixation and lung platelet retention. Restoration of endothelial MHC I rendered MHC I-deficient mice susceptible to lung injury. Neutrophil responses, including neutrophil extracellular trap (NET) release, were intact in endothelial MHC I-deficient mice, whereas complement depletion reduced both lung injury and NETs. Human pulmonary endothelial cells showed high HLA class I expression, and posttransfusion complement activation was increased in clinical TRALI. These results indicate that the critical source of antigen for anti-leukocyte antibodies is in fact the endothelium, which reframes our understanding of TRALI as a rapid-onset vasculitis. Inhibition of complement activation may have multiple beneficial effects of reducing endothelial injury, platelet retention, and NET release in conditions where antibodies trigger these pathogenic responses.
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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.