Trial reportThe Journal of clinical investigation2019
An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup.
Trial report in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01969344 (Subpopulations and Intermediate Outcome Measures in COPD Study), which is not on this map. Cited by 67 papers, 2 of them syntheses 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.
Subpopulations and Intermediate Outcome Measures in COPD Study
Who cites it
67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.
- Biologic therapies targeting type 2 inflammation in chronic obstructive pulmonary disease: a systematic review and meta-analysis of randomised controlled trials.BMJ open respiratory research · 2026Pooled it
- Potential drug targets for chronic obstructive pulmonary disease in the plasma proteome identified through Mendelian randomization.BMC pulmonary medicine · 2025Pooled it
- Dysregulated iron metabolism associates with neutrophilic airway inflammation in COPD.Clinical science (London, England : 1979) · 2026Article
- Treatment of chronic obstructive pulmonary disease: current pipeline and new opportunities.Nature reviews. Drug discovery · 2026Review
- Mucus plugs-associated gene expression identifies pathophysiology shared with chronic bronchitis.American journal of respiratory and critical care medicine · 2026Article
- The airway epithelial-immune axis: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Predominant lung cDC2 phenotype in cigarette smoke-exposed mice favors polarization of IL-17-producing CD4American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Inhaled Targeted Nano-Drug Delivery Systems for COPD: Precision Solutions to Clinical Barriers.International journal of nanomedicine · 2026Review
- Targeting the gut-lung axis in COPD: from microbial metabolites to fecal microbiota transplantation.Frontiers in microbiology · 2026Review
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Fueling the fire in the lung-brain axis: The salience network connects allergen-provoked TH17 responses to psychological stress in asthma.Brain, behavior, and immunity · 2025Article
- Clinical and Biological Features of a Thickened Basement Membrane Zone in Asthma.American journal of respiratory and critical care medicine · 2025Article
- Clinical and Pathophysiological Tangles Between Allergy and Autoimmunity: Deconstructing an Old Dichotomic Paradigm.Clinical reviews in allergy & immunology · 2025Review
- Increased Muc5AC and Decreased Ciliated Cells in Severe Asthma Partially Restored by Inhibition of IL-4Rα Receptor.American journal of respiratory and critical care medicine · 2024Article
- Neutrophils in nasal polyps exhibit transcriptional adaptation and proinflammatory roles that depend on local polyp milieu.JCI insight · 2024Article
- A new Anticalin protein for IL-23 inhibits non-type 2 allergen-driven mouse lung inflammation and airway hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Design of the SPIROMICS Study of Early COPD Progression: SOURCE Study.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2024Article
- Peripheral Blood Mononuclear Cell Gene Expression Associated with Pulmonary Microvascular Perfusion: The Multi-Ethnic Study of Atherosclerosis Chronic Obstructive Pulmonary Disease.Annals of the American Thoracic Society · 2024Article
- RETRACTED: Involvement of GPR43 Receptor in Effect ofNutrients · 2024Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
27 authors at 15 institutions in 2 countries.
Funding
Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a heterogeneous smoking-related disease characterized by airway obstruction and inflammation. This inflammation may persist even after smoking cessation and responds variably to corticosteroids. Personalizing treatment to biologically similar "molecular phenotypes" may improve therapeutic efficacy in COPD. IL-17A is involved in neutrophilic inflammation and corticosteroid resistance, and thus may be particularly important in a COPD molecular phenotype.
methodsWe generated a gene expression signature of IL-17A response in bronchial airway epithelial brushings from smokers with and without COPD (n = 238), and validated it using data from 2 randomized trials of IL-17 blockade in psoriasis. This IL-17 signature was related to clinical and pathologic characteristics in 2 additional human studies of COPD: (a) SPIROMICS (n = 47), which included former and current smokers with COPD, and (b) GLUCOLD (n = 79), in which COPD participants were randomized to placebo or corticosteroids.
resultsThe IL-17 signature was associated with an inflammatory profile characteristic of an IL-17 response, including increased airway neutrophils and macrophages. In SPIROMICS the signature was associated with increased airway obstruction and functional small airways disease on quantitative chest CT. In GLUCOLD the signature was associated with decreased response to corticosteroids, irrespective of airway eosinophilic or type 2 inflammation.
conclusionThese data suggest that a gene signature of IL-17 airway epithelial response distinguishes a biologically, radiographically, and clinically distinct COPD subgroup that may benefit from personalized therapy.
trial registrationClinicalTrials.gov NCT01969344.
fundingPrimary support from the NIH, grants K23HL123778, K12HL11999, U19AI077439, DK072517, U01HL137880, K24HL137013 and R01HL121774 and contracts HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C and HHSN268200900020C.
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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.