ArticleMolecular medicine (Cambridge, Mass.)1998
Requirements for allergen-induced airway hyperreactivity in T and B cell-deficient mice.
Article in Molecular medicine (Cambridge, Mass.), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 241 citations in OpenAlex.
- High-Dimensional Analysis of Type 2 Lymphocyte Dynamics During Mepolizumab or Dupilumab Treatment in Severe Asthma.Allergy · 2025Article
- Innate Immunity and Asthma Exacerbations: Insights From Human Models.Immunological reviews · 2025Review
- Natural antibodies drive type 2 immunity in response to damage-associated molecular patterns.JCI insight · 2024Article
- Immunoglobulin E-Dependent Activation of Immune Cells in Rhinovirus-Induced Asthma Exacerbation.Frontiers in allergy · 2022Article
- Bevacizumab regulates inflammatory cytokines and inhibits VEGFR2 signaling pathway in an ovalbumin-induced rat model of airway hypersensitivity.Inflammopharmacology · 2021Article
- MicroRNA-142-3p inhibits IFN-γ production via targeting of RICTOR inAnnals of translational medicine · 2019Article
- T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.European journal of immunology · 2019Article
- Fungi in Mucoobstructive Airway Diseases.Annals of the American Thoracic Society · 2018Review
- β-Arrestin-2-Dependent Signaling Promotes CCR4-mediated Chemotaxis of Murine T-Helper Type 2 Cells.American journal of respiratory cell and molecular biology · 2018Article
- Development of a mouse model of eosinophilic chronic rhinosinusitis with nasal polyp by nasal instillation of an Aspergillus protease and ovalbumin.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017Article
- Group 2 Innate Lymphoid Cells Exhibit a Dynamic Phenotype in Allergic Airway Inflammation.Frontiers in immunology · 2017Article
- A novel peptide ADAM8 inhibitor attenuates bronchial hyperresponsiveness and Th2 cytokine mediated inflammation of murine asthmatic models.Scientific reports · 2016Article
- The adaptor protein insulin receptor substrate 2 inhibits alternative macrophage activation and allergic lung inflammation.Science signaling · 2016Article
- CD4⁺ and CD8⁺ T cells play a central role in a HDM driven model of allergic asthma.Respiratory research · 2016Article
- Evolution of the Immune Response to Chronic Airway Colonization with Aspergillus fumigatus Hyphae.Infection and immunity · 2015Article
- Leukotriene enhanced allergic lung inflammation through induction of chemokine production.Clinical and experimental medicine · 2015Article
- Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.The Journal of allergy and clinical immunology · 2015Article
- Challenges and Current Efforts in the Development of Biomarkers for Chronic Inflammatory and Remodeling Conditions of the Lungs.Biomarker insights · 2015Review
- B cells play key roles in th2-type airway immune responses in mice exposed to natural airborne allergens.PloS one · 2015Article
- Long-Acting Beta Agonists Enhance Allergic Airway Disease.PloS one · 2015Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe pathogenesis of asthma is believed to reflect antigen-induced airway inflammation leading to the recruitment of eosinophils and activation of mast cells through cell-associated IgE. Controversies persist however, regarding the relative importance of different pathogenic cells and effector molecules. MATERIALS AND
methodsA variety of gene-targeted mice were examined for the induction of cholinergic airway hyperresponsiveness (AH), allergic airway inflammation, mucus production, and serum IgE reactivity following intratracheal challenge with a potent allergen. AH was determined using whole-body plethysmography following acetylcholine challenge. Where possible, results were confirmed using neutralizing antibodies and cell-specific reconstitution of immune deficient mice.
resultsT and B cell-deficient, recombinase-activating-gene-deficient mice (RAG -/-) failed to develop significant allergic inflammation and AH following allergen challenge. Reconstitution of RAG -/- mice with CD4+ T cells alone was sufficient to restore allergen-induced AH, allergic inflammation, and goblet cell hyperplasia, but not IgE reactivity. Sensitized B cell-deficient mice also developed airway hyperreactivity and lung inflammation comparable to that of wild-type animals, confirming that antibodies were dispensable. Treatment with neutralizing anti-IL-4 antibody or sensitization of IL-4-deficient mice resulted in loss of airway hyperreactivity, whereas treatment with anti-IL-5 antibody or sensitization of IL-5-deficient mice had no effect.
conclusionsIn mice, CD4+ T cells are alone sufficient to mediate many of the pathognomonic changes that occur in human asthma by a mechanism dependent upon IL-4, but independent of IL-5, IgE, or both. Clarification of the role played by CD4+ T cells is likely to stimulate important therapeutic advances in treatment of asthma.
Indexed as
Identifiers
9642684PMC2230383W1683039388What 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.