ArticleMucosal immunology2014
Oxidative stress-mediated iNKT-cell activation is involved in COPD pathogenesis.
Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Cytotoxic lymphocytes in COPD airways: increased NK cells associated with disease, iNKT and NKT-like cells with current smoking.Respiratory research · 2018Trial
- Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits.Frontiers in immunology · 2026Review
- The Role of Exhaled Breath Condensate in Chronic Inflammatory and Neoplastic Diseases of the Respiratory Tract.International journal of molecular sciences · 2024Review
- Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.Scientific reports · 2023Article
- Article
- Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023Review
- CD1-mediated immune responses in mucosal tissues: molecular mechanisms underlying lipid antigen presentation system.Experimental & molecular medicine · 2023Review
- Early innate cell interactions withFrontiers in immunology · 2023Review
- Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.Frontiers in cellular and infection microbiology · 2023Review
- Type 1 invariant natural killer T cells in chronic inflammation and tissue fibrosis.Frontiers in immunology · 2023Review
- IL-20 Cytokines Are Involved in Epithelial Lesions Associated with Virus-Induced COPD Exacerbation in Mice.Biomedicines · 2021Article
- An innate contribution of human nicotinic receptor polymorphisms to COPD-like lesions.Nature communications · 2021Article
- Article
- Mucosal Associated Invariant T Cells Were Activated and Polarized Toward Th17 in Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2021Article
- Boosting the IL-22 response using flagellin prevents bacterial infection in cigarette smoke-exposed mice.Clinical and experimental immunology · 2020Article
- Modelling the Impact of Chronic Cigarette Smoke Exposure in Obese Mice: Metabolic, Pulmonary, Intestinal, and Cardiac Issues.Nutrients · 2020Article
- MAIT Cells Come to the Rescue in Cancer Immunotherapy?Cancers · 2020Review
- Senescence in Pulmonary Fibrosis: Between Aging and Exposure.Frontiers in medicine · 2020Review
- [Bronchial dilatations in patients with chronic obstructive pulmonary disease in a Tunisian center: effect on disease progression and prognosis].The Pan African medical journal · 2020Article
- IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis.The European respiratory journal · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a major clinical challenge mostly due to cigarette smoke (CS) exposure. Invariant natural killer T (iNKT) cells are potent immunoregulatory cells that have a crucial role in inflammation. In the current study, we investigate the role of iNKT cells in COPD pathogenesis. The frequency of activated NKT cells was found to be increased in peripheral blood of COPD patients relative to controls. In mice chronically exposed to CS, activated iNKT cells accumulated in the lungs and strongly contributed to the pathogenesis. The detrimental role of iNKT cells was confirmed in an acute model of oxidative stress, an effect that depended on interleukin (IL)-17. CS extracts directly activated mouse and human dendritic cells (DC) and airway epithelial cells (AECs) to trigger interferonγ and/or IL-17 production by iNKT cells, an effect ablated by the anti-oxidant N-acetylcystein. In mice, this treatment abrogates iNKT-cell accumulation in the lung and abolished the development of COPD. Together, activation of iNKT cells by oxidative stress in DC and AECs participates in the development of experimental COPD, a finding that might be exploited at a therapeutic level.
Indexed as
Identifiers
What OpenQuestion holds
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.