ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Role of IL-17A in murine models of COPD airway disease.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Association Between Non-obstructive Chronic Bronchitis and Incident Chronic Obstructive Pulmonary Disease and All-Cause Mortality: A Systematic Review and Meta-Analysis.Frontiers in medicine · 2021Pooled it
- Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk.International journal of molecular sciences · 2026Article
- IL-17A activates the PI3K/AKT/mTOR pathway to regulate bronchial fibroblast autophagy-mediated airway remodeling: evidence from conditional IL-17RA-deficient mice.Frontiers in physiology · 2026Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Innate Lymphoid Cells.Advances in experimental medicine and biology · 2025Review
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- Application and progress of new technologies and new materials in the treatment of pathological scar.Frontiers in chemistry · 2024Review
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types?American journal of respiratory cell and molecular biology · 2023Article
- Impact of protocatechuic acid on alleviation of pulmonary damage induced by cyclophosphamide targeting peroxisome proliferator activator receptor, silent information regulator type-1, and fork head box protein in rats.Inflammopharmacology · 2023Article
- Aging-Related Mechanisms Contribute to Corticosteroid Insensitivity in Elderly Asthma.International journal of molecular sciences · 2023Review
- NCR negative group 3 innate lymphoid cell (NCRImmunity, inflammation and disease · 2023Article
- The forgotten key players in rheumatoid arthritis: IL-8 and IL-17 - Unmet needs and therapeutic perspectives.Frontiers in medicine · 2023Review
- 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
- Dynamic Changes of NCRInflammation · 2022Article
- Cell Type-Specific Roles of STAT3 Signaling in the Pathogenesis and Progression of K-ras Mutant Lung Adenocarcinoma.Cancers · 2022Review
- Oxidative Stress Promotes Corticosteroid Insensitivity in Asthma and COPD.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Leukocyte Function in COPD: Clinical Relevance and Potential for Drug Therapy.International journal of chronic obstructive pulmonary disease · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Small airway fibrosis is a major pathological feature of chronic obstructive pulmonary disease (COPD) and is refractory to current treatments. Chronic inflammatory cells accumulate around small airways in COPD and are thought to play a major role in small airway fibrosis. Mice deficient in α/β T cells have recently been shown to be protected from both experimental airway inflammation and fibrosis. In these models, CD4+Th17 cells and secretion of IL-17A are increased. However, a pathogenic role for IL-17 in specifically mediating fibrosis around airways has not been demonstrated. Here a role for IL-17A in airway fibrosis was demonstrated using mice deficient in the IL-17 receptor A (il17ra) Il17ra-deficient mice were protected from both airway inflammation and fibrosis in two different models of airway fibrosis that employ COPD-relevant stimuli. In these models, CD4+ Th17 are a major source of IL-17A with other expressing cell types including γδ T cells, type 3 innate lymphoid cells, polymorphonuclear cells, and CD8+ T cells. Antibody neutralization of IL-17RA or IL-17A confirmed that IL-17A was the relevant pathogenic IL-17 isoform and IL-17RA was the relevant receptor in airway inflammation and fibrosis. These results demonstrate that the IL-17A/IL-17 RA axis is crucial to murine airway fibrosis. These findings suggest that IL-17 might be targeted to prevent the progression of airway fibrosis in 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 OpenQuestion graph.