ArticleThe Journal of clinical investigation2022
IL-1β-dependent extravasation of preexisting lung-restricted autoantibodies during lung transplantation activates complement and mediates primary graft dysfunction.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Targeting mitochondrial complex I of CD177Cell reports. Medicine · 2025Article
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Biomarkers for primary graft dysfunction after lung transplantation: a review of current evidence and future prospects.Frontiers in physiology · 2025Review
- Contrasting predictors of severe primary graft dysfunction following transplant for chronic and acute respiratory failure.Journal of thoracic disease · 2024Article
- Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.The Journal of clinical investigation · 2024Article
- Temporal correlation between postreperfusion complement deposition and severe primary graft dysfunction in lung allografts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling.The Journal of clinical investigation · 2024Article
- Intestinal microbiota links to allograft stability after lung transplantation: a prospective cohort study.Signal transduction and targeted therapy · 2023Article
- The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction.Frontiers in transplantation · 2023Review
- Ferroptosis in the post-transplantation inflammatory response.Cellular immunologyArticle
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Preexisting lung-restricted autoantibodies (LRAs) are associated with a higher incidence of primary graft dysfunction (PGD), although it remains unclear whether LRAs can drive its pathogenesis. In syngeneic murine left lung transplant recipients, preexisting LRAs worsened graft dysfunction, which was evident by impaired gas exchange, increased pulmonary edema, and activation of damage-associated pathways in lung epithelial cells. LRA-mediated injury was distinct from ischemia-reperfusion injury since deletion of donor nonclassical monocytes and host neutrophils could not prevent graft dysfunction in LRA-pretreated recipients. Whole LRA IgG molecules were necessary for lung injury, which was mediated by the classical and alternative complement pathways and reversed by complement inhibition. However, deletion of Fc receptors in donor macrophages or mannose-binding lectin in recipient mice failed to rescue lung function. LRA-mediated injury was localized to the transplanted lung and dependent on IL-1β-mediated permeabilization of pulmonary vascular endothelium, which allowed extravasation of antibodies. Genetic deletion or pharmacological inhibition of IL-1R in the donor lungs prevented LRA-induced graft injury. In humans, preexisting LRAs were an independent risk factor for severe PGD and could be treated with plasmapheresis and complement blockade. We conclude that preexisting LRAs can compound ischemia-reperfusion injury to worsen PGD for which complement inhibition may be effective.
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