ArticleAmerican journal of respiratory and critical care medicine2010
Chronic cigarette smoke exposure generates pathogenic T cells capable of driving COPD-like disease in Rag2-/- mice.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
- Natural and disease-specific autoantibodies in chronic obstructive pulmonary disease.Clinical and experimental immunology · 2015Trial
- Experimental Mouse Models and Human Lung Organoid Models for Studying Chronic Obstructive Pulmonary Disease.Biomolecules & therapeutics · 2024Review
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
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- Predicting the pulmonary effects of long-term e-cigarette use: are the clouds clearing?European respiratory review : an official journal of the European Respiratory Society · 2022Review
- The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD.Scientific reports · 2021Article
- Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure.Frontiers in molecular biosciences · 2021Article
- MAPK mutations and cigarette smoke promote the pathogenesis of pulmonary Langerhans cell histiocytosis.JCI insight · 2020Article
- Innate Immunity and Cell Surface Receptors in the Pathogenesis of COPD: Insights from Mouse Smoking Models.International journal of chronic obstructive pulmonary disease · 2020Review
- Reduced expression of the Ion channel CFTR contributes to airspace enlargement as a consequence of aging and in response to cigarette smoke in mice.Respiratory research · 2019Article
- COPD beyond proximal bronchial obstruction: phenotyping and related tools at the bedside.European respiratory review : an official journal of the European Respiratory Society · 2019Review
- Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease.Journal of leukocyte biology · 2019Article
- NKG2D Regulation of Lung Pathology and Dendritic Cell Function Following Respiratory Syncytial Virus Infection.The Journal of infectious diseases · 2018Article
- Autoantibodies in Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2018Review
- Blockade of RAGE ameliorates elastase-induced emphysema development and progressionFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Exposure to Ambient Particulate Matter Induced COPD in a Rat Model and a Description of the Underlying Mechanism.Scientific reports · 2017Article
- Experimental animal models for COPD: a methodological review.Tobacco induced diseases · 2017Review
- Article
- The Role of Mitochondria and Oxidative/Antioxidative Imbalance in Pathobiology of Chronic Obstructive Pulmonary Disease.Oxidative medicine and cellular longevity · 2016Review
- Microarray analysis of long non-coding RNAs in COPD lung tissue.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
rationalePathogenic T cells drive, or sustain, a number of inflammatory diseases. Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease associated with the accumulation of activated T cells. We previously demonstrated that chronic cigarette smoke (CS) exposure causes oligoclonal expansion of lung CD4(+) T cells and CD8(+) T cells in a mouse model of COPD, thus implicating these cells in disease pathogenesis.
objectivesTo determine whether T cells are pathogenic in a CS-induced mouse model of COPD.
methodsWe transferred lung CD3(+) T cells from filtered air (FA)- and CS-exposed mice into Rag2(-/-) recipients. Endpoints associated with the COPD phenotype were then measured. MEASUREMENTS AND MAIN
resultsHere, we demonstrate that chronic CS exposure generates pathogenic T cells. Transfer of CD3(+) T cells from the lungs of CS-exposed mice into Rag2(-/-) recipients led to substantial pulmonary changes pathognomonic of COPD. These changes included monocyte/macrophage and neutrophil accumulation, increased expression of cytokines and chemokines, activation of proteases, apoptosis of alveolar epithelial cells, matrix degradation, and airspace enlargement reminiscent of emphysema.
conclusionsThese data formally demonstrate, for the first time, that chronic CS exposure leads to the generation of pathogenic T cells capable of inducing COPD-like disease in Rag2(-/-) mice. This report provides novel insights into COPD pathogenesis.
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