ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Dectin-1 and IL-17A suppress murine asthma induced by Aspergillus versicolor but not Cladosporium cladosporioides due to differences in β-glucan surface exposure.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 37 citations in OpenAlex.
- The immune response of upper and lower airway epithelial cells to Aspergillus fumigatus and Candida albicans-derived β-glucan in Th17 type cytokine environment.Archives of microbiology · 2025Article
- Characterization of fungal exposure and dectin-1 expression in healthy horses and horses with severe asthma.American journal of veterinary research · 2022Article
- First Characterization and Description ofJournal of fungi (Basel, Switzerland) · 2021Article
- Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model.Scientific reports · 2021Article
- Environmental exposures and mechanisms in allergy and asthma development.The Journal of clinical investigation · 2019Review
- Environment and Host-Genetic Determinants in Early Development of Allergic Asthma: Contribution of Fungi.Frontiers in immunology · 2019Review
- Dysregulated invertebrate tropomyosin-dectin-1 interaction confers susceptibility to allergic diseases.Science immunology · 2018Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- C-Type Lectin Receptors in Asthma.Frontiers in immunology · 2018Review
- β-Glucan exacerbates allergic asthma independent of fungal sensitization and promotes steroid-resistant TThe Journal of allergy and clinical immunology · 2017Article
- Generation and Characterization of Indoor Fungal Aerosols for Inhalation Studies.Applied and environmental microbiology · 2016Article
- Collaborative interactions between type 2 innate lymphoid cells and antigen-specific CD4+ Th2 cells exacerbate murine allergic airway diseases with prominent eosinophilia.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Immune responses to airborne fungi and non-invasive airway diseases.Seminars in immunopathology · 2015Review
- Article
- Co-recognition of β-glucan and chitin and programming of adaptive immunity to Aspergillus fumigatus.Frontiers in microbiology · 2015Article
- Innate receptors and cellular defense against pulmonary infections.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- The mycobiota: interactions between commensal fungi and the host immune system.Nature reviews. Immunology · 2014Review
- Comparison of the interleukin-1β-inducing potency of allergenic spores from higher fungi (basidiomycetes) in a cryopreserved human whole blood system.International archives of allergy and immunology · 2014Article
- Fungal glycan interactions with epithelial cells in allergic airway disease.Current opinion in microbiology · 2013Review
- Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides.The Journal of allergy and clinical immunology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
There is considerable evidence supporting a role for mold exposure in the pathogenesis and expression of childhood asthma. Aspergillus versicolor and Cladosporium cladosporioides are common molds that have been implicated in asthma. In a model of mold-induced asthma, mice were repeatedly exposed to either A. versicolor or C. cladosporioides spores. The two molds induced distinct phenotypes, and this effect was observed in both BALB/c and C57BL/6 strains. C. cladosporioides induced robust airway hyperresponsiveness (AHR), eosinophilia, and a predominately Th2 response, whereas A. versicolor induced a strong Th17 response and neutrophilic inflammation, but very mild AHR. Neutralization of IL-17A resulted in strong AHR and eosinophilic inflammation following A. versicolor exposure. In Dectin-1-deficient mice, A. versicolor exposure resulted in markedly attenuated IL-17A and robust AHR compared with wild-type mice. In contrast, C. cladosporioides induced AHR and eosinophilic inflammation independent of IL-17A and Dectin-1. A. versicolor, but not C. cladosporioides, spores had increased exposure of β-glucans on their surface and were able to bind Dectin-1. Thus, the host response to C. cladosporioides was IL-17A- and Dectin-1-independent, whereas Dectin-1- and IL-17A-dependent pathways were protective against the development of asthma after exposure to A. versicolor.
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