ArticleJCI insight2024
Tuft cells are required for a rhinovirus-induced asthma phenotype in immature mice.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 10 citations in OpenAlex.
- Influenza-induced tuft cell expansion is associated with changes in ILC2 populations in the distal lungs of mice.Physiological reports · 2026Article
- Influenza-induced tuft cell expansion alters ILC-mediated inflammation.bioRxiv : the preprint server for biology · 2026Article
- Protective or pathogenic? Tuft cells shape divergent immune outcomes in helminth and viral infections.Current opinion in immunology · 2025Review
- Rhinovirus C15 infection induces airway epithelial cell remodeling and robust inflammatory responses: Potential implications for airway obstruction in children.Mucosal immunology · 2025Article
- Beyond cysts - organization of epithelial networks in the murine thymus.Journal of cell science · 2025Article
- The immunology of asthma.Nature immunology · 2025Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.Frontiers in immunology · 2025Review
- Tuft cell cysteinyl leukotrienes are necessary for rhinovirus-induced mucus metaplasia, type 2 inflammation and airway hyperresponsiveness in immature mice.Frontiers in immunology · 2025Article
- Epithelial-neuronal-immune cell interactions: Implications for immunity, inflammation, and tissue homeostasis at mucosal sites.The Journal of allergy and clinical immunology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Infection of immature mice with rhinovirus (RV) induces an asthma-like phenotype consisting of type 2 inflammation, mucous metaplasia, eosinophilic inflammation, and airway hyperresponsiveness that is dependent on IL-25 and type 2 innate lymphoid cells (ILC2s). Doublecortin-like kinase 1-positive (DCLK1+) tuft cells are a major source of IL-25. We sought to determine the requirement of tuft cells for the RV-induced asthma phenotype in wild-type mice and mice deficient in Pou2f3, a transcription factor required for tuft cell development. C57BL/6J mice infected with RV-A1B on day 6 of life and RV-A2 on day 13 of life showed increased DCLK1+ tuft cells in the large airways. Compared with wild-type mice, RV-infected Pou2f3-/- mice showed reductions in IL-25 mRNA and protein expression, ILC2 expansion, type 2 cytokine expression, mucous metaplasia, lung eosinophils, and airway methacholine responsiveness. We conclude that airway tuft cells are required for the asthma phenotype observed in immature mice undergoing repeated RV infections. Furthermore, RV-induced tuft cell development provides a mechanism by which early-life viral infections could potentiate type 2 inflammatory responses to future infections.
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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.