ArticleAmerican journal of respiratory and critical care medicine2016
NOX2 Activation of Natural Killer T Cells Is Blocked by the Adenosine A2A Receptor to Inhibit Lung Ischemia-Reperfusion Injury.
Article in American journal of respiratory and critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- The Role of NADPH Oxidase 2 in Leukocytes.Antioxidants (Basel, Switzerland) · 2025Review
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Global trends and frontiers in iNKT cells: a bibliometric and visualized analysis.Frontiers in immunology · 2025Article
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Resolution of post-lung transplant ischemia-reperfusion injury is modulated via Resolvin D1-FPR2 and Maresin 1-LGR6 signaling.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Article
- Immune response associated with ischemia and reperfusion injury during organ transplantation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.Journal of inflammation research · 2022Review
- Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review.Transplantation direct · 2021Review
- Single Nucleotide Polymorphisms of IL-33 Gene Correlated with Renal Allograft Fibrosis in Kidney Transplant Recipients.Journal of immunology research · 2021Article
- Minimizing Ischemia Reperfusion Injury in Xenotransplantation.Frontiers in immunology · 2021Review
- Case Report: Can Inhaled Adenosine Attenuate COVID-19?Frontiers in pharmacology · 2021Article
- MicroRNA-206 antagomiR‒enriched extracellular vesicles attenuate lung ischemia‒reperfusion injury through CXCL1 regulation in alveolar epithelial cells.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2020Article
- Nitrite attenuates mitochondrial impairment and vascular permeability induced by ischemia-reperfusion injury in the lung.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- SPECT imaging of lung ischemia-reperfusion injury using [American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Metabolic Triggers of Invariant Natural Killer T-Cell Activation during Sterile Autoinflammatory Disease.Critical reviews in immunology · 2020Review
- Lung Innate Lymphoid Cell Composition Is Altered in Primary Graft Dysfunction.American journal of respiratory and critical care medicine · 2020Article
- Genetic inactivation of the phospholipase AAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Historical and Current Adenosine Receptor Agonists in Preclinical and Clinical Development.Frontiers in cellular neuroscience · 2019Review
- Increasing circulating sphingosine-1-phosphate attenuates lung injury during ex vivo lung perfusion.The Journal of thoracic and cardiovascular surgery · 2018Article
- Pannexin-1 channels on endothelial cells mediate vascular inflammation during lung ischemia-reperfusion injury.American journal of physiology. Lung cellular and molecular physiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
rationaleIschemia-reperfusion (IR) injury after lung transplantation, which affects both short- and long-term allograft survival, involves activation of NADPH oxidase 2 (NOX2) and activation of invariant natural killer T (iNKT) cells to produce IL-17. Adenosine A2A receptor (A2AR) agonists are known to potently attenuate lung IR injury and IL-17 production. However, mechanisms for iNKT cell activation after IR and A2AR agonist-mediated protection remain unclear.
objectivesWe tested the hypothesis that NOX2 mediates IL-17 production by iNKT cells after IR and that A2AR agonism prevents IR injury by blocking NOX2 activation in iNKT cells.
methodsAn in vivo murine hilar ligation model of IR injury was used, in which left lungs underwent 1 hour of ischemia and 2 hours of reperfusion. MEASUREMENTS AND MAIN
resultsAdoptive transfer of iNKT cells from p47(phox-/-) or NOX2(-/-) mice to Jα18(-/-) (iNKT cell-deficient) mice significantly attenuated lung IR injury and IL-17 production. Treatment with an A2AR agonist attenuated IR injury and IL-17 production in wild-type (WT) mice and in Jα18(-/-) mice reconstituted with WT, but not A2AR(-/-), iNKT cells. Furthermore, the A2AR agonist prevented IL-17 production by murine and human iNKT cells after acute hypoxia-reoxygenation by blocking p47(phox) phosphorylation, a critical step for NOX2 activation.
conclusionsNOX2 plays a key role in inducing iNKT cell-mediated IL-17 production and subsequent lung injury after IR. A primary mechanism for A2AR agonist-mediated protection entails inhibition of NOX2 in iNKT cells. Therefore, agonism of A2ARs on iNKT cells may be a novel therapeutic strategy to prevent primary graft dysfunction after lung transplantation.
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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.