ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Expression of IL-4/IL-13 receptors in differentiating human airway epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Th2 cytokine-induced mucociliary remodeling in chronic rhinosinusitis: implications for antiviral defense and epithelial function.Respiratory research · 2026Article
- Targeting IL-13 and IL-4 in Asthma: Therapeutic Implications on Airway Remodeling in Severe Asthma.Clinical reviews in allergy & immunology · 2025Review
- Leptin augments IL-13-induced airway eotaxins and submucosal eosinophilia in obesity-associated asthma.The Journal of allergy and clinical immunology · 2025Article
- Increased Muc5AC and Decreased Ciliated Cells in Severe Asthma Partially Restored by Inhibition of IL-4Rα Receptor.American journal of respiratory and critical care medicine · 2024Article
- Cytokines in Allergic Conjunctivitis: Unraveling Their Pathophysiological Roles.Life (Basel, Switzerland) · 2024Review
- IL-13 deficiency exacerbates lung damage and impairs epithelial-derived type 2 molecules during nematode infection.Life science alliance · 2021Article
- Targeted therapy in eosinophilic chronic obstructive pulmonary disease.ERJ open research · 2021Review
- Interleukin (IL)-13 and IL-17A contribute to neo-osteogenesis in chronic rhinosinusitis by inducing RUNX2.EBioMedicine · 2019Article
- Chemokine expression in the early response to injury in human airway epithelial cells.PloS one · 2018Article
- Tight junctions in pulmonary epithelia during lung inflammation.Pflugers Archiv : European journal of physiology · 2017Review
- Expression of surfactant protein D in airways of asthmatics and interleukin-13 modulation of surfactant protein D in human models of airway epithelium.Respiratory research · 2015Article
- Interleukin-4 and interleukin-13 compromise the sinonasal epithelial barrier and perturb intercellular junction protein expression.International forum of allergy & rhinology · 2014Article
- Cross-roads in the lung: immune cells and tissue interactions as determinants of allergic asthma.Immunologic research · 2012Review
- Gene-gene and gene-environmental interactions of childhood asthma: a multifactor dimension reduction approach.PloS one · 2012Article
- Effects of a polyherbal formulation on inflammation and histopathological alterations in mice with ovalbumin-induced allergic asthma.Avicenna journal of phytomedicineArticle
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Authors and funding
5 authors.
Funding
Abstract
IL-4 and IL-13 elicit several important responses in airway epithelium including chemokine secretion and mucous secretion that may contribute to airway inflammation, cell migration, and differentiation. These cytokines have overlapping but not identical effector profiles likely due to shared subunits in their receptor complexes. These receptors are variably described in epithelial cells, and the relative expression, localization, and function of these receptors in differentiated and repairing epithelial cells are not clear. We examined IL-4/IL-13 receptor expression and localization in primary airway epithelial cells collected from normal human lungs and grown under conditions yielding both undifferentiated and differentiated cells inclusive of basal, goblet, and ciliated cell phenotypes. Gene expression of the IL-4Rα, IL-2Rγc, IL-13Rα1, and IL-13Rα2 receptor subunits increased with differentiation, but different patterns of localization and protein abundance were seen for each subunit based on both differentiation and the cell subtypes present. Increased expression of receptor subunits observed in more differentiated cells was associated with more substantial functional responses to IL-4 stimulation including increased eotaxin-3 expression and accelerated migration after injury. We demonstrate substantial differences in IL-4/IL-13 receptor subunit expression and responsiveness to IL-4 based on the extent of airway epithelial cell differentiation and suggest that these differences may have functional consequences in airway inflammation.
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