ArticleJCI insight2017
IRF5 distinguishes severe asthma in humans and drives Th1 phenotype and airway hyperreactivity in mice.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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
59 citing papers in PubMed, 85 citations in OpenAlex.
- Autophagy functions in lung macrophages and dendritic cells to regulate allergen-dependent inflammatory responses.Autophagy · 2026Article
- Nanozymes as Emerging Therapeutics for Asthma: A Redox-Responsive and Immunomodulatory Strategy.Biomedicines · 2026Review
- Beyond the Usual Suspects: Unmasking Low-T2 Asthma in Children.Journal of clinical medicine · 2026Review
- Evaluating the Influence ofBiomolecules · 2025Article
- Asthma Phenotypes and Biomarkers.Respiratory care · 2025Review
- Rhinovirus as a driver of airway T cell dynamics in children with treatment-refractory recurrent wheeze.JCI insight · 2025Article
- CD8+ TEMRAs in severe asthma associate with asthma symptom duration and escape proliferation arrest.JCI insight · 2025Article
- T1-T2 Interplay in the Complex Immune Landscape of Severe Asthma.Immunological reviews · 2025Review
- Clinical and Pathophysiological Tangles Between Allergy and Autoimmunity: Deconstructing an Old Dichotomic Paradigm.Clinical reviews in allergy & immunology · 2025Review
- Improvement of glucocorticoid sensitivity and attenuation of pulmonary allergic reactions by exogenous supplementation with betaine in HDM and LPS-induced allergic mouse model.Clinical and translational allergy · 2025Article
- Interferon regulatory factor 5: a potential target for therapeutic intervention in inflammatory diseases.Frontiers in immunology · 2025Review
- Identification of potential diagnostic markers and molecular mechanisms of asthma and ulcerative colitis based on bioinformatics and machine learning.Frontiers in molecular biosciences · 2025Article
- Dust mite antigens endow dendritic cells with the capacity to induce a Th2 response by regulating their methylation profiles.Cell communication and signaling : CCS · 2024Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Nuclear receptor corepressor 1 deficiency exacerbates asthma by modulating macrophage polarization.Cell death discovery · 2023Article
- RNA mNature communications · 2023Article
- Leptin/obR signaling exacerbates obesity-related neutrophilic airway inflammation through inflammatory M1 macrophages.Molecular medicine (Cambridge, Mass.) · 2023Article
- CCL5 is a potential bridge between type 1 and type 2 inflammation in asthma.The Journal of allergy and clinical immunology · 2023Article
- Phenotype overlap in the natural history of asthma.European respiratory review : an official journal of the European Respiratory Society · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Severe asthma (SA) is a significant problem both clinically and economically, given its poor response to corticosteroids (CS). We recently reported a complex type 1-dominated (IFN-γ-dominated) immune response in more than 50% of severe asthmatics despite high-dose CS treatment. Also, IFN-γ was found to be critical for increased airway hyperreactivity (AHR) in our model of SA. The transcription factor IRF5 expressed in M1 macrophages can induce a Th1/Th17 response in cocultured human T cells. Here we show markedly higher expression of IRF5 in bronchoalveolar lavage (BAL) cells of severe asthmatics as compared with that in cells from milder asthmatics or healthy controls. Using our SA mouse model, we demonstrate that lack of IRF5 in lymph node migratory DCs severely limits their ability to stimulate the generation of IFN-γ- and IL-17-producing CD4+ T cells and IRF5-/- mice subjected to the SA model displayed significantly lower IFN-γ and IL-17 responses, albeit showing a reciprocal increase in Th2 response. However, the absence of IRF5 rendered the mice responsive to CS with suppression of the heightened Th2 response. These data support the notion that IRF5 inhibition in combination with CS may be a viable approach to manage disease in a subset of severe asthmatics.
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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.