Trial reportThe Journal of clinical investigation1999
Constitutive activation of an epithelial signal transducer and activator of transcription (STAT) pathway in asthma.
Trial report in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 219 citations in OpenAlex.
- Aberrant mucin expression and keratinization distinguishing severe from mild asthma revealed by interpretable machine learning.JCI insight · 2026Article
- Asthma Phenotypes and Biomarkers.Respiratory care · 2025Review
- MOSES: a methylation-based gene association approach for unveiling environmentally regulated genes linked to a trait or disease.Clinical epigenetics · 2024Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Cis- and trans-eQTM analysis reveals novel epigenetic and transcriptomic immune markers of atopic asthma in airway epithelium.The Journal of allergy and clinical immunology · 2023Article
- Pyrroloquinoline Quinone Administration Alleviates Allergic Airway Inflammation in Mice by Regulating the JAK-STAT Signaling Pathway.Mediators of inflammation · 2022Article
- STAT1 epigenetically regulates LCP2 and TNFAIP2 by recruiting EP300 to contribute to the pathogenesis of inflammatory bowel disease.Clinical epigenetics · 2021Article
- Chronic Candida infection, bronchiectasis, immunoglobulin abnormalities, and stunting: a case report of a natural mutation of STAT1 (c.986C>G) in an adolescent male.BMC infectious diseases · 2021Article
- Anti-inflammatory mechanisms of the novel cytokine interleukin-38 in allergic asthma.Cellular & molecular immunology · 2020Article
- Resident alveolar macrophage-derived vesicular SOCS3 dampens allergic airway inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- IFN-stimulated Gene Expression, Type 2 Inflammation, and Endoplasmic Reticulum Stress in Asthma.American journal of respiratory and critical care medicine · 2018Article
- Effects of Allergic Sensitization on Antiviral Immunity: Allergen, Virus, and Host Cell Mechanisms.Current allergy and asthma reports · 2017Review
- The Expression ofTanaffos · 2017Article
- PARP inhibition treatment in a nonconventional experimental mouse model of chronic asthma.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Anti-inflammatory potential of PI3Kδ and JAK inhibitors in asthma patients.Respiratory research · 2016Article
- [Expression profiles of PI3K, NF-κB, and STAT1 in peripheral blood mononuclear cells in children with bronchial asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Current concepts of severe asthma.The Journal of clinical investigation · 2016Review
- Effect of the plant derivative Compound A on the production of corticosteroid-resistant chemokines in airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2015Article
- IFN-γ-induced JAK/STAT, but not NF-κB, signaling pathway is insensitive to glucocorticoid in airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- D prostanoid receptor 2 (chemoattractant receptor-homologous molecule expressed on TH2 cells) protein expression in asthmatic patients and its effects on bronchial epithelial cells.The Journal of allergy and clinical immunology · 2015Article
4 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
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokine effects on immunity and inflammation often depend on the transcription factors termed signal transducers and activators of transcription (STATs), so STAT signaling pathways are candidates for influencing inflammatory disease. We reasoned that selective IFN responsiveness of the first STAT family member (Stat1) and Stat1-dependent immune-response genes such as intercellular adhesion molecule-1 (ICAM-1), IFN regulatory factor-1 (IRF-1), and Stat1 itself in airway epithelial cells provides a basis for detecting cytokine signaling abnormalities in inflammatory airway disease. On the basis of nuclear localization and phosphorylation, we found that epithelial Stat1 (but not other control transcription factors) was invariably activated in asthmatic compared with normal control or chronic bronchitis subjects. Furthermore, epithelial levels of activated Stat1 correlated with levels of expression for epithelial ICAM-1, IRF-1, and Stat1, and in turn, ICAM-1 levels correlated with T-cell accumulation in tissue. However, only low levels of IFN-gamma or IFN-gamma-producing cells were detected in airway tissue in all subjects. The results therefore provide initial evidence linking abnormal behavior of STAT pathways for cytokine signaling to the development of an inflammatory disease. In that context, the results also change the current scheme for asthma pathogenesis to one that must include a localized gain in transcriptional signal ordinarily used for a T helper 1-type cytokine (IFN-gamma) in combination with allergy-driven overproduction of T helper 2-type cytokines.
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.