ArticleJournal of immunology (Baltimore, Md. : 1950)2012
MAPK regulation of IL-4/IL-13 receptors contributes to the synergistic increase in CCL11/eotaxin-1 in response to TGF-β1 and IL-13 in human airway fibroblasts.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 54 citations in OpenAlex.
- Trial
- Improvement of Mixed Inflammatory Environment in Nasal Secretions of Diffuse Type 2 Chronic Rhinosinusitis With Nasal Polyps Under Dupilumab.Clinical and translational allergy · 2026Article
- PEBP1 and 15-LO-1 in Asthma: Biomarker Potential for Diagnosis and Severity Stratification.Diagnostics (Basel, Switzerland) · 2025Article
- Leptin augments IL-13-induced airway eotaxins and submucosal eosinophilia in obesity-associated asthma.The Journal of allergy and clinical immunology · 2025Article
- Effect of formononetin on progressive pulmonary pathologies: multitarget mechanisms and therapeutic prospects.Frontiers in pharmacology · 2025Review
- Anti-asthmatic miR-224-5p inhibits the FHL1/MAPK pathway to repress airway smooth muscle cell proliferation in a murine model of asthma-like airway inflammation.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022Article
- NF-κB perturbation reveals unique immunomodulatory functions in Prx1Science translational medicine · 2022Article
- Induction of Severe Eosinophilic Esophagitis and Multi-Organ Inflammation by Airborne Allergens is Associated with IL-4/IL-13 and CCL11 but Not IgE in Genetic Susceptible Mice.Journal of inflammation research · 2022Article
- Eosinophil-Mediated Immune Control of Adult Filarial Nematode Infection Can Proceed in the Absence of IL-4 Receptor Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Formononetin Attenuates Airway Inflammation and Oxidative Stress in Murine Allergic Asthma.Frontiers in pharmacology · 2020Article
- The influence of PMExperimental and therapeutic medicine · 2019Article
- A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue.The Journal of experimental medicine · 2019Article
- Regulation of CBL and ESR1 expression by microRNA-22‑3p, 513a-5p and 625-5p may impact the pathogenesis of dust mite-induced pediatric asthma.International journal of molecular medicine · 2016Article
- An Overlook to the Characteristics and Roles Played by Eotaxin Network in the Pathophysiology of Food Allergies: Allergic Asthma and Atopic Dermatitis.Inflammation · 2016Review
- Article
- IL-13 receptor α2 is a negative prognostic factor in human lung cancer and stimulates lung cancer growth in mice.Oncotarget · 2015Article
- Commentary: IL-4 and IL-13 receptors and signaling.Cytokine · 2015Article
- Leukotriene enhanced allergic lung inflammation through induction of chemokine production.Clinical and experimental medicine · 2015Article
- Angiotensin-(1-7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation.British journal of pharmacology · 2015Article
- Interleukin-13 induces collagen type-1 expression through matrix metalloproteinase-2 and transforming growth factor-β1 in airway fibroblasts in asthma.The European respiratory journal · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
CCL11/eotaxin-1 is a potent eosinophilic CC chemokine expressed by primary human fibroblasts. The combination of TGF-β1 and IL-13 synergistically increases CCL11 expression, but the mechanisms behind the synergy are unclear. To address this, human airway fibroblast cultures from normal and asthmatic subjects were exposed to IL-13 alone or TGF-β1 plus IL-13. Transcriptional (nuclear run-on) and posttranscriptional (mRNA stability) assays confirmed that transcriptional regulation is critical for synergistic expression of CCL11. TGF-β1 plus IL-13 synergistically increased STAT-6 phosphorylation, nuclear translocation, and binding to the CCL11 promoter as compared with IL-13 alone. STAT-6 small interfering RNA significantly knocked down both STAT-6 mRNA expression and phosphorylation and inhibited CCL11 mRNA and protein expression. Regulation of the IL-4Rα complex by TGF-β1 augmented IL-13 signaling by dampening IL-13Rα2 expression, overcoming IL-13's autoregulation of its pathway and enhancing the expression of CCL11. Our data suggest that TGF-β1 induced activation of the MEK/ERK pathway reduces IL-13Rα2 expression induced by IL-13. Thus, TGF-β1, a pleiotropic cytokine upregulated in asthmatic airways, can augment eosinophilic inflammation by interfering with IL-13's negative feedback autoregulatory loop under MEK/ERK-dependent conditions.
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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.