ArticleThe Journal of experimental medicine2011
MHC class I-specific antibody binding to nonhematopoietic cells drives complement activation to induce transfusion-related acute lung injury in mice.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 100 citations in OpenAlex.
- Mouse Models of Transfusion-Related Acute Lung Injury (TRALI).Methods in molecular biology (Clifton, N.J.) · 2026Article
- Inhibition of terminal complement complex formation alleviates murine antibody-mediated TRALI.Blood · 2025Article
- Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.The Journal of clinical investigation · 2024Article
- IgG hexamers initiate acute lung injury.bioRxiv : the preprint server for biology · 2024Article
- Sex-specific NLRP3 activation in neutrophils promotes neutrophil recruitment and NETosis in the murine model of diffuse alveolar hemorrhage.Frontiers in immunology · 2024Article
- Mechanism and intervention of murine transfusion-related acute lung injury caused by anti-CD36 antibodies.JCI insight · 2023Article
- Update on transfusion-related acute lung injury: an overview of its pathogenesis and management.Frontiers in immunology · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Synergistic Protection against Secondary Pneumococcal Infection by Human Monoclonal Antibodies Targeting Distinct Epitopes.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment-From Mice to Men.Biomedicines · 2022Review
- Platelets as Key Factors in Inflammation: Focus on CD40L/CD40.Frontiers in immunology · 2022Review
- Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice.Blood advances · 2021Article
- Transfusion of target antigens to preimmunized recipients: a new mechanism in transfusion-related acute lung injury.Blood advances · 2021Article
- The Immune System in Transfusion-Related Acute Lung Injury Prevention and Therapy: Update and Perspective.Frontiers in molecular biosciences · 2021Review
- Complement activation on endothelium initiates antibody-mediated acute lung injury.The Journal of clinical investigation · 2020Article
- Evaluation of Platelet Responses in Transfusion-Related Acute Lung Injury (TRALI).Transfusion medicine reviews · 2020Review
- Biological and structural characterization of murine TRALI antibody reveals increased Fc-mediated complement activation.Blood advances · 2020Article
- Incompatible erythrocyte transfusion with lipopolysaccharide induces acute lung injury in a novel rat model.PloS one · 2020Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transfusion-related acute lung injury (TRALI), a form of noncardiogenic pulmonary edema that develops during or within 6 h after a blood transfusion, is the most frequent cause of transfusion-associated death in the United States. Because development of TRALI is associated with donor antibodies (Abs) reactive with recipient major histocompatibility complex (MHC), a mouse model has been studied in which TRALI-like disease is caused by injecting mice with anti-MHC class I monoclonal Ab (mAb). Previous publications with this model have concluded that disease is caused by FcR-dependent activation of neutrophils and platelets, with production of reactive oxygen species that damage pulmonary vascular endothelium. In this study, we confirm the role of reactive oxygen species in the pathogenesis of this mouse model of TRALI and show ultrastructural evidence of pulmonary vascular injury within 5 min of anti-MHC class I mAb injection. However, we demonstrate that disease induction in this model involves macrophages rather than neutrophils or platelets, activation of complement and production of C5a rather than activation of FcγRI, FcγRIII, or FcγRIV, and binding of anti-MHC class I mAb to non-BM-derived cells such as pulmonary vascular endothelium. These observations have important implications for the prevention and treatment of TRALI.
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