ArticleThe Journal of experimental medicine1996
Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity.
Article in The Journal of experimental medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 175 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
175 citing papers in PubMed, 727 citations in OpenAlex.
- The FOXA transcription factors in allergic airway disease and asthma.Frontiers in allergy · 2026Review
- TSLP Production Induced by Poly(I:C) Stimulation Increased in the Presence of Th2 Cytokines in Patients with Severe ECRS.International archives of otorhinolaryngology · 2025Article
- A current review on animal models of anti-asthmatic drugs screening.Frontiers in pharmacology · 2025Review
- Immunological factors, important players in the development of asthma.BMC immunology · 2024Review
- Brainstem DbhNature · 2024Article
- Diacylglycerol kinase is a keystone regulator of signaling relevant to the pathophysiology of asthma.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Defining and targeting mechanisms of eosinophilic inflammation in a new era of severe asthma treatment.The Journal of clinical investigation · 2024Review
- Immunologic aspects of asthma: from molecular mechanisms to disease pathophysiology and clinical translation.Frontiers in immunology · 2024Review
- Virus-like Particle Vaccine Expressing the Respiratory Syncytial Virus Pre-Fusion and G Proteins Confers Protection against RSV Challenge Infection.Pharmaceutics · 2023Article
- Effect of Biologic Therapies on Airway Hyperresponsiveness and Allergic Response: A Systematic Literature Review.Journal of asthma and allergy · 2023Review
- Distinct spatial and temporal roles for Th1, Th2, and Th17 cells in asthma.Frontiers in immunology · 2022Review
- Behavior of Eosinophil Counts in Recovered and Deceased COVID-19 Patients over the Course of the Disease.Viruses · 2021Article
- Review
- Emerging concepts and directed therapeutics for the management of asthma: regulating the regulators.Inflammopharmacology · 2021Review
- Aspirin Actions in Treatment of NSAID-Exacerbated Respiratory Disease.Frontiers in immunology · 2021Review
- Are We Meeting the Promise of Endotypes and Precision Medicine in Asthma?Physiological reviews · 2020Review
- The Heterogeneity, Origins, and Impact of Migratory iILC2 Cells in Anti-helminth Immunity.Frontiers in immunology · 2020Review
- Diacylglycerol kinase ζ promotes allergic airway inflammation and airway hyperresponsiveness through distinct mechanisms.Science signaling · 2019Article
- Proinflammatory Pathways in the Pathogenesis of Asthma.Clinics in chest medicine · 2019Review
- Fungi in Mucoobstructive Airway Diseases.Annals of the American Thoracic Society · 2018Review
115 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Reversible airway hyperreactivity underlies the pathophysiology of asthma, yet the precise mediators of the response remain unclear. Human studies have correlated aberrant activation of T helper (Th) 2-like effector systems in the airways with disease. A murine model of airway hyperreactivity in response to acetylcholine was established using mice immunized with ovalbumin and challenged with aerosolized antigen. No airway hyperractivity occurred in severe combined immunodeficient mice. Identically immunized BALB/c mice developed an influx of cells, with a predominance of eosinophils and CD4+ T cells, into the lungs and bronchoalveolar lavage fluid at the time that substantial changes in airway pressure and resistance were quantitated. Challenged animals developed marked increases in Th2 cytokine production, eosinophil influx, and serum immunoglobulin E levels. Neutralization of interleukin (IL) 4 using monoclonal antibodies administered during the period of systemic immunization abrogated airway hyperractivity but had little effect on the influx of eosinophils. Administration of anti-IL-4 only during the period of the aerosol challenge did not affect the subsequent response to acetylcholine. Finally, administration of anti-IL-5 antibodies at levels that suppressed eosinophils to < 1% of recruited cells had no effect on the subsequent airway responses. BALB/c mice had significantly greater airway responses than C57BL/6 mice, consistent with enhanced IL-4 responses to antigen in BALB/c mice. Taken together, these data implicate IL-4 generated during the period of lymphocyte priming with antigen in establishing the cascade of responses required to generate airway hyperractivity to inhaled antigen. No role for IL-5 or eosinophils could be demonstrated.
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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.