ArticleThe Journal of allergy and clinical immunology2014
Signaling through FcRγ-associated receptors on dendritic cells drives IL-33-dependent TH2-type responses.
Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- α‑Cyperone targets the PAK1‑JNK/NF‑κB axis to modulate dendritic cells maturation and Th2/Th9 differentiation in an asthma model.International journal of molecular medicine · 2026Article
- The IL-33/ST2 pathway to modulate the inflammatory microenvironment: A new therapeutic target in chronic obstructive pulmonary disease.Biochemistry and biophysics reports · 2026Review
- Myeloid-derived IL-33 drives γδ T cell-dependent resistance against cutaneous infection by Strongyloides ratti.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Review
- Dendritic cells drive profibrotic inflammation and aberrant T cell polarization in systemic sclerosis.Rheumatology (Oxford, England) · 2023Article
- Gastric alarmin release: A warning signal in the development of gastric mucosal diseases.Frontiers in immunology · 2022Review
- Cellular context of IL-33 expression dictates impact on anti-helminth immunity.Science immunology · 2020Article
- Article
- Ozone-induced enhancement of airway hyperreactivity in rhesus macaques: Effects of antioxidant treatment.The Journal of allergy and clinical immunology · 2020Article
- Allergic inflammation is initiated by IL-33-dependent crosstalk between mast cells and basophils.PloS one · 2020Article
- Mimicking Antigen-Driven Asthma in Rodent Models-How Close Can We Get?Frontiers in immunology · 2020Review
- Group 2 Innate Lymphoid Cells (ILC2): Type 2 Immunity and Helminth Immunity.International journal of molecular sciences · 2019Review
- Trefoil Factor 2 Promotes Type 2 Immunity and Lung Repair through Intrinsic Roles in Hematopoietic and Nonhematopoietic Cells.The American journal of pathology · 2018Article
- Dectin-2 Is a C-Type Lectin Receptor that Recognizes Pneumocystis and Participates in Innate Immune Responses.American journal of respiratory cell and molecular biology · 2018Article
- CD209a Synergizes with Dectin-2 and Mincle to Drive Severe Th17 Cell-Mediated Schistosome Egg-Induced Immunopathology.Cell reports · 2018Article
- Interleukin-33 in Systemic Sclerosis: Expression and Pathogenesis.Frontiers in immunology · 2018Review
- Fas Signaling in Dendritic Cells Mediates Th2 Polarization in HDM-Induced Allergic Pulmonary Inflammation.Frontiers in immunology · 2018Article
- C-Type Lectin Receptors in Asthma.Frontiers in immunology · 2018Review
- Dephosphorylated Polymerase I and Transcript Release Factor Prevents Allergic Asthma Exacerbations by Limiting IL-33 Release.Frontiers in immunology · 2018Article
- Pathogenic CD4The Journal of allergy and clinical immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough allergic sensitization can be generated against various allergens, it is unknown how such a diversity of antigens is able to promote TH2-mediated inflammation leading to atopy. Our previous studies demonstrated that allergen-specific IgG immune complexes (ICs) and house dust mite (HDM) extract both induced dendritic cells (DCs) to drive TH2-mediated inflammation, but the mechanism by which these diverse stimuli produce similar responses is unknown.
objectiveWe sought to identify the DC signaling pathways used by TH2 stimuli to promote TH2-mediated inflammation.
methodsC57BL/6, FcγRIII(-/-), FcRγ(-/-), and ST2(-/-) mice were sensitized and challenged with HDM, and inflammation was assessed based on results of flow cytometry and histology and cytokine production. Bone marrow-derived DCs from these strains were used in signaling and adoptive transfer experiments.
resultsOur findings indicate that 2 distinct TH2 stimuli, ICs and HDM, use the FcRγ-associated receptors FcγRIII and Dectin-2, respectively, to promote TH2-mediated lung inflammation. In this study we demonstrate that both ICs and HDM induce expression of IL-33, a critical mediator in asthma pathogenesis and the differentiation of TH2 cells, in DCs. Upregulation of IL-33 in DCs is dependent on FcRγ, Toll-like receptor 4, and phosphoinositide 3-kinase. Exogenous IL-33 is sufficient to restore the development of TH2 responses in FcRγ-deficient mice. Finally, adoptive transfer of allergen-pulsed FcRγ(+/-) bone-marrow derived DCs restores the development of TH2-type inflammation in FcRγ-deficient mice, demonstrating the necessity of this signaling pathway in DCs for allergen-induced inflammation.
conclusionThese data identify a mechanism whereby TH2 stimuli signal through FcRγ-associated receptors on DCs to upregulate IL-33 production and induce TH2-mediated allergic airway inflammation.
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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.