ArticleJCI insight2017
Eosinophils promote inducible NOS-mediated lung allograft acceptance.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Activation of donor-derived eosinophils during static storage contributes to primary graft dysfunction after lung transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Innate lymphoid cells: unsung heroes or villains in multiple sclerosis pathogenesis?Immunologic research · 2026Review
- Unique Immune Polarization of the Lung Allograft: Implications for Organ-specific Immunoregulation and Tolerance Induction.Transplantation · 2026Review
- Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Review
- Lung adenocarcinoma-derived IFN-γ promotes growth by modulating CD8+ T cell production of CCR5 chemokines.The Journal of clinical investigation · 2025Article
- Maintenance of graft tissue-resident Foxp3+ cells is necessary for lung transplant tolerance in mice.The Journal of clinical investigation · 2025Article
- Chronic Lung Allograft Dysfunction: Clinical Manifestations and Immunologic Mechanisms.Transplantation · 2025Review
- Correlation between obstructive sleep apnea and serum markers HIF-1, IL-6 and iNOS after lung transplantation.Sleep & breathing = Schlaf & Atmung · 2024Article
- Stress-induced eosinophil activation contributes to postoperative morbidity and mortality after lung resection.Science translational medicine · 2024Article
- IL-33: Friend or foe in transplantation?The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024Review
- PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms.Molecular biology reports · 2024Review
- Smoking exposure-induced bronchus-associated lymphoid tissue in donor lungs does not prevent tolerance induction after transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- BAL Fluid Eosinophilia Associates With Chronic Lung Allograft Dysfunction Risk: A Multicenter Study.Chest · 2023Article
- Protective and pathogenic functions of innate lymphoid cells in transplantation.Clinical and experimental immunology · 2023Review
- Adaptive Immunosuppression in Lung Transplant Recipients Applying Complementary Biomarkers: The Zurich Protocol.Medicina (Kaunas, Lithuania) · 2023Article
- The innate immune brakes of the lung.Frontiers in immunology · 2023Review
- Ischemia reperfusion injury facilitates lung allograft acceptance through IL-33-mediated activation of donor-derived IL-5 producing group 2 innate lymphoid cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- Differential regulation of Type 1 and Type 2 mouse eosinophil activation by apoptotic cells.Frontiers in immunology · 2022Article
- Screening and identification of key regulatory connections and immune cell infiltration characteristics for lung transplant rejection using mucosal biopsies.International immunopharmacology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Lungs allografts have worse long-term survival compared with other organ transplants. This is most likely due to their unique immunoregulation that may not respond to traditional immunosuppression. For example, local NO generation by inducible NOS (iNOS) is critical for lung allograft acceptance but associates with rejection of other solid organs. The source of NO in accepting lung allografts remains unknown. Here, we report that, unlike the case for other pulmonary processes in which myeloid cells control NO generation, recipient-derived eosinophils play a critical and nonredundant role in iNOS-mediated lung allograft acceptance. Depletion of eosinophils reduces NO levels to that of recipients with global deletion of iNOS and leads to a costimulatory blockade-resistant form of rejection. Furthermore, NO production by eosinophils depends on Th1 polarization by inflammatory mediators, such as IFN-γ and TNF-α. Neutralization of such mediators abrogates eosinophil suppressive capacity. Our data point to what we believe to be a unique and previously unrecognized role of eosinophil polarization in mediating allograft tolerance and put into perspective the use of high-dose eosinophil-ablating corticosteroids after lung transplantation.
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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.