ArticleThe Journal of allergy and clinical immunology2012
Dendritic cells and alveolar macrophages mediate IL-13-induced airway inflammation and chemokine production.
Article in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Influenza A/PR8 virus infection in mice suppresses basal and Oncostatin M-induced IL-33 expression in vivo and in vitro.Scientific reports · 2026Article
- Type 2 conventional dendritic cells and regulatory T cells form a barrier tissue circuit to control allergic inflammation.bioRxiv : the preprint server for biology · 2026Article
- Pollutant particles enhance house dust mite induced type 2 inflammation and the recruitment of monocyte derived Cd11cParticle and fibre toxicology · 2026Article
- Cell-Specific Contribution of IL-4 Receptor α Signaling Shapes the Overall Manifestation of Allergic Airway Disease.American journal of respiratory cell and molecular biology · 2024Article
- Outcome of SARS-CoV-2 reinfection depends on genetic background in female mice.Nature communications · 2024Article
- CCL11 released by GSDMD-mediated macrophage pyroptosis regulates angiogenesis after hindlimb ischemia.Cell death discovery · 2024Article
- IL-13 promotes functional recovery after myocardial infarction via direct signaling to macrophages.JCI insight · 2024Article
- Host immune responses associated with SARS-CoV-2 Omicron infection result in protection or pathology during reinfection depending on mouse genetic background.Research square · 2023Article
- SUMOylation of Rho-associated protein kinase 2 induces goblet cell metaplasia in allergic airways.Nature communications · 2023Article
- Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium.Diseases (Basel, Switzerland) · 2022Article
- Conditional depletion of macrophages ameliorates cholestatic liver injury and fibrosis via lncRNA-H19.Cell death & disease · 2021Article
- Macrophages: The Good, the Bad, and the Gluttony.Frontiers in immunology · 2021Review
- Fibroblast activation protein-targeted-4-1BB ligand agonist amplifies effector functions of intratumoral T cells in human cancer.Journal for immunotherapy of cancer · 2020Article
- Therapeutic and prophylactic deletion of IL-4Ra-signaling ameliorates established ovalbumin induced allergic asthma.Allergy · 2020Article
- The Role of T Cells and Macrophages in Asthma Pathogenesis: A New Perspective on Mutual Crosstalk.Mediators of inflammation · 2020Article
- Inhibition of the dipeptidyl peptidase DPP4 (CD26) reveals IL-33-dependent eosinophil-mediated control of tumor growth.Nature immunology · 2019Article
- Eosinophil recruitment is dynamically regulated by interplay among lung dendritic cell subsets after allergen challenge.Nature communications · 2018Article
- Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-β-Activated Kinase 1/MAP3K7-Binding Protein 2.Allergy, asthma & immunology research · 2018Article
- IL-34 and CSF-1 display an equivalent macrophage differentiation ability but a different polarization potential.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIL-13 in the airway induces pathologies that are highly characteristic of asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inflammation. As such, it is important to identify the IL-13-responding cell types that mediate each of the above pathologies. For example, IL-13's effects on epithelium contribute to mucus metaplasia and AHR. IL-13's effects on smooth muscle also contribute to AHR. However, it has been difficult to identify the cell types that mediate IL-13-induced airway inflammation.
objectiveWe sought to determine which cell types mediate IL-13-induced airway inflammation.
methodsWe treated the airways of mice with IL-13 alone or in combination with IFN-γ. We associated the inhibitory effect of IFN-γ on IL-13-induced airway inflammation and chemokine production with cell types in the lung that coexpress IL-13 and IFN-γ receptors. We then evaluated IL-13-induced responses in CD11c promoter-directed diphtheria toxin receptor-expressing mice that were depleted of both dendritic cells and alveolar macrophages and in CD11b promoter-directed diphtheria toxin receptor-expressing mice that were depleted of dendritic cells.
resultsDendritic cell and alveolar macrophage depletion protected mice from IL-13-induced airway inflammation and CCL11, CCL24, CCL22, and CCL17 chemokine production. Preferential depletion of dendritic cells protected mice from IL-13-induced airway inflammation and CCL22 and CCL17 chemokine production but not from IL-13-induced CCL11 and CCL24 chemokine production. In either case mice were not protected from IL-13-induced AHR and mucus metaplasia.
conclusionsPulmonary dendritic cells and alveolar macrophages mediate IL-13-induced airway inflammation and chemokine production.
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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.