ArticleInfection and immunity2011
Necessary and sufficient role for T helper cells to prevent fungal dissemination in allergic lung disease.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Selective Targeting of IL-1RAP-Dependent Eosinophilic Inflammation in Allergic Fungal Airway Disease.Allergy · 2026Article
- Allergic Fungal Rhinosinusitis Diagnosis, Management, Associated Conditions, Pathophysiology, and Future Directions: Summary of a Multidisciplinary Workshop.International forum of allergy & rhinology · 2025Review
- Mgl2Nature communications · 2025Article
- Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation.Frontiers in allergy · 2025Review
- Host gastric corpus microenvironment facilitates Ascaris suum larval hatching and infection in a murine model.PLoS neglected tropical diseases · 2024Article
- Severe influenza A virus pneumonia complicated withFrontiers in cellular and infection microbiology · 2023Article
- Review
- Cytoskeletal Alteration Is an Early Cellular Response in Pulmonary Epithelium Infected with Aspergillus fumigatus Rather than Scedosporium apiospermum.Microbial ecology · 2022Article
- STAT6 Blockade AbrogatesFrontiers in immunology · 2022Article
- Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice.PLoS neglected tropical diseases · 2021Article
- Candida albicans elicits protective allergic responses via platelet mediated T helper 2 and T helper 17 cell polarization.Immunity · 2021Article
- Novel acute hypersensitivity pneumonitis model induced by airway mycosis and high dose lipopolysaccharide.Respiratory research · 2021Article
- Airway Mycosis and the Regulation of Type 2 Immunity.Journal of fungi (Basel, Switzerland) · 2020Review
- Caspase-11 promotes allergic airway inflammation.Nature communications · 2020Article
- Selective cleavage of fibrinogen by diverse proteinases initiates innate allergic and antifungal immunity through CD11b.The Journal of biological chemistry · 2019Article
- Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits.Nature communications · 2019Article
- Environment and Host-Genetic Determinants in Early Development of Allergic Asthma: Contribution of Fungi.Frontiers in immunology · 2019Review
- Fungi in Mucoobstructive Airway Diseases.Annals of the American Thoracic Society · 2018Review
- Host response to pulmonary fungal infections: A highlight on cell-driven immunity toCurrent pharmacology reports · 2017Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mucosal immune responses to fungal infection range from T helper type 2 (Th2) cell-directed allergic inflammation to Th1-predominant neutrophilic inflammation, but the mechanisms directing these divergent mucosal immune outcomes and the role of T cells in host defense against mucosal fungal infections are not known. Here we examined the mouse mucosal immune responses to 12 filamentous environmental fungal species over a broad range of exposure doses and determined the requirement of T cells for host defense. For all tested fungi, low-grade conidium exposures induced Th2- and eosinophil-predominant allergic lung disease, whereas higher exposures led to rapid conversion to neutrophil- and Th1 cell-predominant inflammation, a phenomenon we term immune phenotype switching. All fungal exposure doses were further linked to the secretion of interleukin-17A (IL-17A). Fungal infections with Curvularia lunata and Aspergillus fumigatus were typically confined to the airway during allergic inflammation but became locally invasive and disseminated to the brain at higher conidium challenge doses, in association with predominant Th1 responses. Fungal dissemination occurred at relatively low challenge doses with the conidia of Aspergillus fumigatus administered to recombinase activating gene 1 (Rag-1)-deficient mice, which lack B and T cells, but B cell-deficient μMT mice and T helper cell-reconstituted Rag-1-deficient mice were comparable to wild-type mice in preventing fungal dissemination. Our findings demonstrate that Th2 cell-predominant allergic responses followed by immune phenotype switching and fungal dissemination are highly predictable outcomes with progressive fungal infectious burdens and that T helper cell responses are protective against lethal fungal dissemination.
Indexed as
Identifiers
What OpenQuestion holds
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.