ArticlemBio2013
Complement component 3C3 and C3a receptor are required in chitin-dependent allergic sensitization to Aspergillus fumigatus but dispensable in chitin-induced innate allergic inflammation.
Article in mBio, 2013. 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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- GM000287 is a conserved determinant of serum resistance and virulence in Klebsiella pneumoniae.PLoS pathogens · 2026Article
- Chitin Is a Potent Inducer of Type 2 Airway Inflammation Independent of Endogenous Chitinolytic Activity.Allergy · 2026Article
- Airway sympathectomy attenuates inflammation, transcriptional ratios of Muc5ac and Muc5b, and airway mechanic deficits in mice delivered intranasal IL-13.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Complement's involvement in allergic Th2 immunity: a cross-barrier perspective.The Journal of clinical investigation · 2025Review
- Development and validation of a clinical prediction model forFrontiers in medicine · 2025Article
- Fungal chitin is not an independent mediator of allergic fungal asthma severity.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Chitin Biosynthesis inJournal of fungi (Basel, Switzerland) · 2023Review
- Genome-scale CRISPR screening reveals that C3aR signaling is critical for rapid capture of fungi by macrophages.PLoS pathogens · 2022Article
- Fungal-mediated lung allergic airway disease: The critical role of macrophages and dendritic cells.PLoS pathogens · 2022Review
- Chitinase 3-like-1 protects airway function despite promoting type 2 inflammation during fungal-associated allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Chitinase-Induced Airway Hyperreactivity and Inflammation in a Mouse Model of Nonallergic Asthma.International archives of allergy and immunology · 2021Article
- Differential Interactions of Serum and Bronchoalveolar Lavage Fluid Complement Proteins with Conidia of Airborne Fungal Pathogen Aspergillus fumigatus.Infection and immunity · 2020Article
- Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces.European journal of immunology · 2020Review
- Mechanisms of PathogenicFrontiers in cellular and infection microbiology · 2020Review
- β-1,3-glucan-lackingVirulence · 2019Article
- Article
- Chitin and Its Effects on Inflammatory and Immune Responses.Clinical reviews in allergy & immunology · 2018Review
- Immune Recognition of Fungal Polysaccharides.Journal of fungi (Basel, Switzerland) · 2017Review
- Co-recognition of β-glucan and chitin and programming of adaptive immunity to Aspergillus fumigatus.Frontiers in microbiology · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Levels of the anaphylatoxin C3a are increased in patients with asthma compared with those in nonasthmatics and increase further still during asthma exacerbations. However, the role of C3a during sensitization to allergen is poorly understood. Sensitization to fungal allergens, such as Aspergillus fumigatus, is a strong risk factor for the development of asthma. Exposure to chitin, a structural polysaccharide of the fungal cell wall, induces innate allergic inflammation and may promote sensitization to fungal allergens. Here, we found that coincubation of chitin with serum or intratracheal administration of chitin in mice resulted in the generation of C3a. We established a model of chitin-dependent sensitization to soluble Aspergillus antigens to test the contribution of complement to these events. C3(-/-) and C3aR(-/-) mice were protected from chitin-dependent sensitization to Aspergillus and had reduced lung eosinophilia and type 2 cytokines and serum IgE. In contrast, complement-deficient mice were not protected against chitin-induced innate allergic inflammation. In sensitized mice, plasmacytoid dendritic cells from complement-deficient animals acquired a tolerogenic profile associated with enhanced regulatory T cell responses and suppressed Th2 and Th17 responses specific for Aspergillus. Thus, chitin induces the generation of C3a in the lung, and chitin-dependent allergic sensitization to Aspergillus requires C3aR signaling, which suppresses regulatory dendritic cells and T cells and induces allergy-promoting T cells.
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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.