ArticlePLoS pathogens2015
Respiratory Syncytial Virus Disease Is Mediated by Age-Variable IL-33.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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Who cites it
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.
- The Human Immune Response to Respiratory Syncytial Virus Infection.Clinical microbiology reviews · 2017Pooled it
- Innate Lymphoid Cells Activation and Transcriptomic Changes in Response to Human Dengue Infection.Frontiers in immunology · 2021Trial
- Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.European journal of pediatrics · 2026Review
- MurineCyto-Det: A High-Resolution Murine BALF Cytology Dataset for Leukocyte Segmentation and Detection.bioRxiv : the preprint server for biology · 2026Article
- Early-life viral infection generates pathological tissue-resident memory cells that contribute to asthma-like disease.JCI insight · 2026Article
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- The Complexity of Immunoglobulin A Immune Responses in Respiratory Syncytial Virus Infection.Viruses · 2026Review
- CXCL13 and IL-33 as Immunomodulatory Adjuvants Combined with Respiratory Syncytial Virus Fusion (RSV F) Protein to Enhance Mucosal RSV Vaccination.Infection and drug resistance · 2026Review
- The role of virus in nasal inflammation.European journal of medical research · 2025Review
- Early-life viral infections and asthma: new cells and ideas.Current opinion in pediatrics · 2025Review
- Epithelial Memory After Respiratory Viral Infection in Mice Results in Prolonged Enhancement of Antigen Presentation.Allergy · 2025Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Early-life RSV infection modulates innate immune events, preferentially enhancing allergen-induced type 2 lung inflammation in females.PLoS pathogens · 2025Article
- hMPV Outbreaks: Worldwide Implications of a Re-Emerging Respiratory Pathogen.Microorganisms · 2025Review
- Article
- Comparison of immune responses to respiratory syncytial virus in infancy, childhood, and adulthood using an in vitro model of human respiratory infection.ImmunoHorizons · 2025Article
- Long-term alterations in lung epithelial cells after EL-RSV infection exacerbate allergic responses through IL-1β-induced pathways.Mucosal immunology · 2024Article
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
- Comparative transcriptomic and proteomic kinetic analysis of adeno-associated virus production systems.Applied microbiology and biotechnology · 2024Article
- Diverging patterns in innate immunity against respiratory viruses during a lifetime: lessons from the young and the old.European respiratory review : an official journal of the European Respiratory Society · 2024Review
49 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Respiratory syncytial virus (RSV) is the most common cause of infant hospitalizations and severe RSV infections are a significant risk factor for childhood asthma. The pathogenic mechanisms responsible for RSV induced immunopathophysiology remain elusive. Using an age-appropriate mouse model of RSV, we show that IL-33 plays a critical role in the immunopathogenesis of severe RSV, which is associated with higher group 2 innate lymphoid cells (ILC2s) specifically in neonates. Infection with RSV induced rapid IL-33 expression and an increase in ILC2 numbers in the lungs of neonatal mice; this was not observed in adult mice. Blocking IL-33 with antibodies or using an IL-33 receptor knockout mouse during infection was sufficient to inhibit RSV immunopathogenesis (i.e., airway hyperresponsiveness, Th2 inflammation, eosinophilia, and mucus hyperproduction); whereas administration of IL-33 to adult mice during RSV infection was sufficient to induce RSV disease. Additionally, elevated IL-33 and IL-13 were observed in nasal aspirates from infants hospitalized with RSV; these cytokines declined during convalescence. In summary, IL-33 is necessary, either directly or indirectly, to induce ILC2s and the Th2 biased immunopathophysiology observed following neonatal RSV infection. This study provides a mechanism involving IL-33 and ILC2s in RSV mediated human asthma.
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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.