ArticleInflammation2016
Infiltration of IL-17-Producing T Cells and Treg Cells in a Mouse Model of Smoke-Induced Emphysema.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Genetic Factors Interact With Tobacco Smoke to Modify Risk for Inflammatory Bowel Disease in Humans and Mice.Gastroenterology · 2017Pooled it
- CXCL11 levels regulate lung Treg responses to deter the onset of HIV-related COPD.Respiratory research · 2026Article
- Relationship between systemic immune response index (SIRI) and COPD: a cross-sectional study based on NHANES 2007-2012.Scientific reports · 2025Article
- Effector Tc17 cells resist shift from OXPHOS to aerobic glycolysis.Frontiers in immunology · 2025Article
- Downregulation ofeLife · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- The association of systemic immune-inflammation index with lung function, risk of COPD and COPD severity: A population-based study.PloS one · 2024Article
- L-Arginine, as an essential amino acid, is a potential substitute for treating COPD via regulation of ROS/NLRP3/NF-κB signaling pathway.Cell & bioscience · 2023Article
- Cigarette Smoke Modulates Inflammation and ImmunityAntioxidants & redox signaling · 2023Review
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- NCR negative group 3 innate lymphoid cell (NCRImmunity, inflammation and disease · 2023Article
- The role of Th17 cells: explanation of relationship between periodontitis and COPD?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial-mesenchymal transition in COPD mice.BMC pulmonary medicine · 2021Article
- Enhanced lung inflammatory response in whole-body compared to nose-only cigarette smoke-exposed mice.Respiratory research · 2021Article
- Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence.Frontiers in immunology · 2021Review
- Th17/Treg imbalance in COPD development: suppressors of cytokine signaling and signal transducers and activators of transcription proteins.Scientific reports · 2020Article
- Transition Metal Containing Particulate Matter Promotes Th1 and Th17 Inflammatory Response by Monocyte Activation in Organic and Inorganic Compounds Dependent Manner.International journal of environmental research and public health · 2020Article
- How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?International journal of chronic obstructive pulmonary disease · 2020Review
- Interleukin-17A Deficiency Attenuated Emphysema and Bone Loss in Mice Exposed to Cigarette Smoke.International journal of chronic obstructive pulmonary disease · 2020Article
- [Research Progress of Treg/Th17 in the Treatment of Chronic Obstructive Pulmonary Disease with Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory disease associated with the accumulation of activated T cells. To date, there is little information concerning the intrinsic association among Th17, Tc17, and regulatory T (Treg) cells in COPD. The objective of this study was to investigate the variation of lungs CD4(+)Foxp3(+) Treg cells and IL-17-producing CD4 and CD8 (Th17 and Tc17) lymphocytes in mice with cigarette-induced emphysema. Groups of mice were exposed to cigarette smoke or room air. At weeks 12 and 24, mice were sacrificed to observe histological changes by HE stain. The frequencies of Th17 (CD4(+)IL-17(+)T), Tc17 (CD8(+)IL-17(+)T), and Treg (CD4(+)Foxp3(+)T) cells in lungs from these mice were analyzed by flow cytometry. The mRNA levels of orphan nuclear receptor ROR γt and Foxp3 were performed by real-time quantitative polymerase chain reaction. The protein levels of interleukin-17 (IL-17), IL-6, IL-10, and transforming growth factor-beta (TGF-β1) were measured by enzyme-linked immunosorbent assay. Cigarette smoke caused substantial enlargement of the air spaces accompanied by the destruction of the normal alveolar architecture and led to emphysema. The frequencies of Th17 and Tc17 cells, as well as the expressions of IL-6, IL-17, TGF-β1, and ROR γt were greater in the lungs of cigarette smoke (CS)-exposed mice, particularly in the 24-week CS-exposed mice. The frequencies of Treg cells and the expressions of IL-10 and Foxp3 were lower in CS-exposed mice compared to control group. More important, the frequencies of Tregs were negatively correlated with Th17 cells and with Tc17 cells. Interestingly, a significant portion of the cells that infiltrate the lungs was skewed towards a Tc17 phenotype. Our findings suggest the contribution of Th17, Tc17, and Treg cells in the pathogenesis of COPD. Rebalance of these cells will be helpful for developing and refining the new immunological therapies for COPD.
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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 Socratic graph.