ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Gene expression patterns of Th2 inflammation and intercellular communication in asthmatic airways.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 164 citations in OpenAlex.
- Trial
- Airway remodelling rather than cellular infiltration characterizes both type2 cytokine biomarker-high and -low severe asthma.Allergy · 2022Trial
- Gene network approach reveals co-expression patterns in nasal and bronchial epithelium.Scientific reports · 2019Trial
- Pharmacokinetic/Pharmacodynamic Modelling of Receptor Internalization with CRTH2 Antagonists to Optimize Dose Selection.Clinical pharmacokinetics · 2016Trial
- Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle cells and promote their proliferation by increased extracellular matrix proteins production in asthma.BMC pulmonary medicine · 2016Trial
- Asthma-COPD overlap. Clinical relevance of genomic signatures of type 2 inflammation in chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2015Trial
- The effects of lebrikizumab in patients with mild asthma following whole lung allergen challenge.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2014Trial
- Network analysis identifies a putative role for the PPAR and type 1 interferon pathways in glucocorticoid actions in asthmatics.BMC medical genomics · 2012Trial
- Article
- Guominkang formula alleviates airway inflammation in HDM-induced asthma mice by regulating Wnt/β-Catenin pathway.Chinese medicine · 2026Article
- TGF-β and IL-4 + IL-13 induce neuroplasticity in anFrontiers in immunology · 2026Article
- Type 2 immune responses are associated with less severe COVID-19 in a hospitalized cohort.The journal of allergy and clinical immunology. Global · 2025Article
- Frequent exacerbator-a novel endotype of pediatric asthma.The Journal of allergy and clinical immunology · 2025Review
- Type 2 gene expression signature in severe asthma associates with more advanced airway remodeling.Clinical and translational allergy · 2025Article
- CD4Frontiers in immunology · 2025Review
- Selective HDAC8 inhibition by PCI-34051 attenuates inflammation and airway remodeling in asthmaJournal of translational internal medicine · 2024Article
- Omics approaches in asthma research: Challenges and opportunities.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Grandmaternal allergen sensitization reprograms epigenetic and airway responses to allergen in second-generation offspring.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Acute HDM exposure shows time-of-day and sex-based differences in the severity of lung inflammation and circadian clock disruption.The journal of allergy and clinical immunology. Global · 2023Article
- Identification of candidate aberrant differentially methylated/expressed genes in asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022Article
18 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
11 authors at 4 institutions in 4 countries.
Funding
Abstract
Asthma is canonically thought of as a disorder of excessive Th2-driven inflammation in the airway, although recent studies have described heterogeneity with respect to asthma pathophysiology. We have previously described distinct phenotypes of asthma based on the presence or absence of a three-gene "Th2 signature" in bronchial epithelium, which differ in terms of eosinophilic inflammation, mucin composition, subepithelial fibrosis, and corticosteroid responsiveness. In the present analysis, we sought to describe Th2 inflammation in human asthmatic airways quantitatively with respect to known mediators of inflammation and intercellular communication. Using whole-genome microarray and quantitative real-time PCR analysis of endobronchial biopsies from 27 mild-to-moderate asthmatics and 13 healthy controls with associated clinical and demographic data, we found that asthmatic Th2 inflammation is expressed over a variable continuum, correlating significantly with local and systemic measures of allergy and eosinophilia. We evaluated a composite metric describing 79 coexpressed genes associated with Th2 inflammation against the biological space comprising cytokines, chemokines, and growth factors, identifying distinctive patterns of inflammatory mediators as well as Wnt, TGF-β, and platelet-derived growth factor family members. This integrated description of the factors regulating inflammation, cell migration, and tissue remodeling in asthmatic airways has important consequences for the pathophysiological and clinical impacts of emerging asthma therapeutics targeting Th2 inflammation.
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.