ArticleJCI insight2023
Mechanism and intervention of murine transfusion-related acute lung injury caused by anti-CD36 antibodies.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Ferroptosis-associated changes in transfusion-related acute lung injury in Sprague Dawley rats.Open medicine (Warsaw, Poland) · 2026Article
- Molecular Mechanisms of Transfusion-Associated Immunomodulation and Its Impact in the Critically Ill.International journal of molecular sciences · 2025Review
- Inhibition of terminal complement complex formation alleviates murine antibody-mediated TRALI.Blood · 2025Article
- Brain-penetrant complement inhibition mitigates neurodegeneration in an Alzheimer's disease mouse model.Brain : a journal of neurology · 2025Article
- Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The importance of disrupting complement activation in acute lung injury.The Journal of clinical investigation · 2024Article
- Peimine ameliorates LPS-induced acute lung injury by regulating Nrf2 and NF-κB pathways.American journal of translational research · 2024Article
- Successful allogeneic hematopoietic stem cell transplantation in a patient with type I CD36 deficiency: a case study and literature review.International journal of hematology · 2023Review
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-CD36 Abs have been suggested to induce transfusion-related acute lung injury (TRALI) upon blood transfusion, particularly in Asian populations. However, little is known about the pathological mechanism of anti-CD36 Ab-mediated TRALI, and potential therapies have not yet been identified. Here, we developed a murine model of anti-CD36 Ab-mediated TRALI to address these questions. Administration of mouse mAb against CD36 (mAb GZ1) or human anti-CD36 IgG, but not GZ1 F(ab')2 fragments, induced severe TRALI in Cd36+/+ male mice. Predepletion of recipient monocytes or complement, but not neutrophils or platelets, prevented the development of murine TRALI. Moreover, plasma C5a levels after TRALI induction by anti-CD36 Abs increased more than 3-fold, implying a critical role of complement C5 activation in the mechanism of Fc-dependent anti-CD36-mediated TRALI. Administration of GZ1 F(ab')2, antioxidant (N-acetyl cysteine, NAC), or C5 blocker (mAb BB5.1) before TRALI induction completely protected mice from anti-CD36-mediated TRALI. Although no significant amelioration in TRALI was observed when mice were injected with GZ1 F(ab')2 after TRALI induction, significant improvement was achieved when mice were treated postinduction with NAC or anti-C5. Importantly, anti-C5 treatment completely rescued mice from TRALI, suggesting the potential role of existing anti-C5 drugs in the treatment of patients with TRALI caused by anti-CD36.
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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.