ArticleRespiratory research2011
Antigen-Specific IgG ameliorates allergic airway inflammation via Fcγ receptor IIB on dendritic cells.
Article in Respiratory research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Subcutaneous immunotherapy-induced IgG1 suppresses allergic airway inflammation through FcγRIIb-mediated inhibition of group 2 innate lymphoid cell proliferation.The World Allergy Organization journal · 2026Article
- Best in Class: IgG as a Treatable Trait for Exacerbation Prevention in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2025Article
- The B Cell Response and Formation of Allergenic and Anti-Allergenic Antibodies in Food Allergy.Biology · 2023Review
- Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model.International journal of molecular sciences · 2020Article
- Mimicking Antigen-Driven Asthma in Rodent Models-How Close Can We Get?Frontiers in immunology · 2020Review
- Mouse Model of Cat Allergic Rhinitis and Intranasal Liposome-Adjuvanted Refined Fel d 1 Vaccine.PloS one · 2016Article
- Article
- Molecular basis for downregulation of C5a-mediated inflammation by IgG1 immune complexes in allergy and asthma.Current allergy and asthma reports · 2013Review
- The contribution of allergen-specific IgG to the development of th2-mediated airway inflammation.Journal of allergy · 2012Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere have been few reports on the role of Fc receptors (FcRs) and immunoglobulin G (IgG) in asthma. The purpose of this study is to clarify the role of inhibitory FcRs and antigen presenting cells (APCs) in pathogenesis of asthma and to evaluate antigen-transporting and presenting capacity by APCs in the tracheobronchial mucosa.
methodsIn FcγRIIB deficient (KO) and C57BL/6 (WT) mice, the effects of intratracheal instillation of antigen-specific IgG were analysed using the model with sensitization and airborne challenge with ovalbumin (OVA). Thoracic lymph nodes instilled with fluorescein-conjugated OVA were analysed by fluorescence microscopy. Moreover, we analysed the CD11c+ MHC class II+ cells which intaken fluorescein-conjugated OVA in thoracic lymph nodes by flow cytometry. Also, lung-derived CD11c+ APCs were analysed by flow cytometry. Effects of anti-OVA IgG1 on bone marrow dendritic cells (BMDCs) in vitro were also analysed. Moreover, in FcγRIIB KO mice intravenously transplanted dendritic cells (DCs) differentiated from BMDCs of WT mice, the effects of intratracheal instillation of anti-OVA IgG were evaluated by bronchoalveolar lavage (BAL).
resultsIn WT mice, total cells and eosinophils in BAL fluid reduced after instillation with anti-OVA IgG1. Anti-OVA IgG1 suppressed airway inflammation in hyperresponsiveness and histology. In addition, the number of the fluorescein-conjugated OVA in CD11c+ MHC class II+ cells of thoracic lymph nodes with anti-OVA IgG1 instillation decreased compared with PBS. Also, MHC class II expression on lung-derived CD11c+ APCs with anti-OVA IgG1 instillation reduced. Moreover, in vitro, we showed that BMDCs with anti-OVA IgG1 significantly decreased the T cell proliferation. Finally, we demonstrated that the lacking effects of anti-OVA IgG1 on airway inflammation on FcγRIIB KO mice were restored with WT-derived BMDCs transplanted intravenously.
conclusionAntigen-specific IgG ameliorates allergic airway inflammation via FcγRIIB on DCs.
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Registered trials
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