ArticleAmerican journal of respiratory cell and molecular biology2013
Pulmonary natural killer T cells play an essential role in mediating hyperoxic acute lung injury.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Protective and Immunomodulatory Functions of Exogenous B Cells in Experimental Hyperoxic Lung Injury.Anesthesia and analgesia · 2026Article
- The P2X7 receptor in mucosal adaptive immunity.Purinergic signalling · 2024Review
- Hypoxia-adenosine axis as therapeutic targets for acute respiratory distress syndrome.Frontiers in immunology · 2024Review
- Interplay of hypoxia-inducible factors and oxygen therapy in cardiovascular medicine.Nature reviews. Cardiology · 2023Review
- Extracellular mitochondria drive CD8 T cell dysfunction in trauma by upregulating CD39.Thorax · 2023Article
- Angiotensin-(1-7) alleviates acute lung injury by activating the Mas receptor in neutrophil.Annals of translational medicine · 2022Article
- Implications of Hyperoxia over the Tumor Microenvironment: An Overview Highlighting the Importance of the Immune System.Cancers · 2022Review
- Therapeutic Targeting of Hypoxia-A2-Adenosinergic Pathway in COVID-19 Patients.Physiology (Bethesda, Md.) · 2022Article
- Synapomorphic features of hepatic and pulmonary vasculatures include comparable purinergic signaling responses in host defense and modulation of inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Targeting alveolar-specific succinate dehydrogenase A attenuates pulmonary inflammation during acute lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Hyperoxia and modulation of pulmonary vascular and immune responses in COVID-19.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Case Report: Can Inhaled Adenosine Attenuate COVID-19?Frontiers in pharmacology · 2021Article
- Hypoxia and HIF Signaling: One Axis with Divergent Effects.International journal of molecular sciences · 2020Review
- Ectonucleotidase Modulation of Lymphocyte Function in Gut and Liver.Frontiers in cell and developmental biology · 2020Review
- Therapeutic effects of adenosine in high flow 21% oxygen aereosol in patients with Covid19-pneumonia.PloS one · 2020Article
- Purinergic Signaling in Pulmonary Inflammation.Frontiers in immunology · 2019Review
- Ectonucleotidases in Intestinal and Hepatic Inflammation.Frontiers in immunology · 2019Review
- The ectonucleotidases CD39 and CD73: Novel checkpoint inhibitor targets.Immunological reviews · 2017Review
- NOX2 Activation of Natural Killer T Cells Is Blocked by the Adenosine A2A Receptor to Inhibit Lung Ischemia-Reperfusion Injury.American journal of respiratory and critical care medicine · 2016Article
- Purinergic regulation of the immune system.Nature reviews. Immunology · 2016Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Critically ill patients are routinely exposed to high concentrations of supplemental oxygen for prolonged periods of time, which can be life-saving in the short term, but such exposure also causes severe lung injury and increases mortality. To address this therapeutic dilemma, we studied the mechanisms of the tissue-damaging effects of oxygen in mice. We show that pulmonary invariant natural killer T (iNKT) cells are unexpectedly crucial in the development of acute oxygen-induced lung injury. iNKT cells express high concentrations of the ectonucleotidase CD39, which regulates their state of activation. Both iNKT cell-deficient (Jα18(-/-)) and CD39-null mice tolerate hyperoxia, compared with wild-type control mice that exhibit severe lung injury. An adoptive transfer of wild-type iNKT cells into Jα18(-/-) mice results in hyperoxic lung injury, whereas the transfer of CD39-null iNKT cells does not. Pulmonary iNKT cell activation and proliferation are modulated by ATP-dependent purinergic signaling responses. Hyperoxic lung injury can be induced by selective P2X7-receptor blockade in CD39-null mice. Our data indicate that iNKT cells are involved in the pathogenesis of hyperoxic lung injury, and that tissue protection can be mediated through ATP-induced P2X7 receptor signaling, resulting in iNKT cell death. In conclusion, our data suggest that iNKT cells and purinergic signaling should be evaluated as potential novel therapeutic targets to prevent hyperoxic lung injury.
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