ArticleCells2023
Interaction of Interleukin-17A with a Th2 Response in a Mouse Model of Allergic Airway Inflammation.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Soluble gp130 inhibits Th17 polarization in neutrophilic asthma by blocking IL-6Frontiers in immunology · 2026Article
- A Mixture of Four Probiotic Strains (Probiatop®) Mitigates Food Allergy to Ovalbumin in Mice.Probiotics and antimicrobial proteins · 2025Article
- Ferulic Acid Attenuated Interleukin-17A-Induced Lung Inflammation by Modulating Interleukin-17 Signaling and Tissue Remodeling in a Mouse Model.ACS pharmacology & translational science · 2025Article
- Prostaglandin FThe Journal of veterinary medical science · 2025Article
- Comparative Immunomodulatory Efficacy of Secukinumab and Honokiol in Experimental Asthma and Acute Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Therapeutic effects of a combination ofFrontiers in nutrition · 2025Article
- Targeting Common Inflammatory Mediators in Experimental Severe Asthma and Acute Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundA total of 262 million people worldwide suffer from asthma and 461000 people died from it in 2019. Asthma is a disease with different endotypes defined by the granulocytes found in the asthmatic lung. In allergic asthma, the eosinophilic endotype is present, driven by a TH2 response. A TH17 immune response leads to the neutrophil endotype. This often causes uncontrolled asthma and is triggered by pollutants, microbes, and oxidative stress. It has been described that a significant number of patients with eosinophilic asthma develop mixed granulocytic asthma over time. The severity of asthma in the mixed endotype is related to the proportion of neutrophils in the lungs. PURPOSE: In this report, we address the question of how a TH2 response interacts with IL-17A in allergic asthma.
methodsTo this end, we used a mouse model to induce allergic asthma followed by an aerosol challenge with ovalbumin. To investigate the role of IL-17A, we administered IL-17A intranasally during the challenge phase.
resultsIL-17A alone did not elicit an immune response, whereas in combination with allergic asthma, it resulted in a shift of the asthmatic endotype from eosinophilic to neutrophilic. TGFβ1 was increased in these lungs compared to asthmatic lungs without IL-17A, as was the expression of the IL-17A receptor subunits IL-17RA and IL-17RC. In cultures with human cells, we also found that IL-17A increased the expression of its receptors only in combination with IL-13. We also found this effect for IL-8, which attracts neutrophils in humans.
conclusionsThe TH2 response increased the sensitivity to IL-17A in a mouse asthma model as well as in human cell lines.
Indexed as
Identifiers
What OpenQuestion holds
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.