Evidence map›Paper›PMID 22933634›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

The β-glucan receptor dectin-1 promotes lung immunopathology during fungal allergy via IL-22.

Lauren M Lilly, Melissa A Gessner, Chad W Dunaway, Allison E Metz, Lisa Schwiebert, Casey T Weaver, Gordon D Brown, Chad Steele

Open access · bronzeAbstract read
In one paragraph

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 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 124 citations in OpenAlex.

  1. How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Fungal chitin is not an independent mediator of allergic fungal asthma severity.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  9. Article
  10. Hematopoietic 12/15-lipoxygenase activity negatively contributes to fungal-associated allergic asthma.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Pathophysiological Role of Vimentin Intermediate Filaments in Lung Diseases.Frontiers in cell and developmental biology · 2022
    Review
  19. Article
  20. Review

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Lauren M LillyDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Melissa A Gessner
Chad W Dunaway
Allison E Metz
Lisa Schwiebert
Casey T Weaver
Gordon D Brown
Chad Steele
University of Alabama at Birmingham · USUniversity of Aberdeen · GB

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Pulmonary defense against aspergillus fumigatus R01HL096702 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STEELE, CHAD · 2010 to 2013
$1.6M
Dectin-1 and Invasive Pulmonary AspergillosisR01AI068917 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STEELE, CHAD · 2009 to 2010
$732k
NHLBI NIH HHS HL096702NHLBI NIH HHS R01 HL096702NIAID NIH HHS AI068917NIAID NIH HHS R01 AI068917NIAMS NIH HHS P30 AR048311
6 · The paper itself

Abstract

Sensitization to fungi, such as the mold Aspergillus fumigatus, is increasingly becoming linked with asthma severity. We have previously shown that lung responses generated via the β-glucan receptor Dectin-1 are required for lung defense during acute, invasive A. fumigatus infection. Unexpectedly, in an allergic model of chronic lung exposure to live A. fumigatus conidia, β-glucan recognition via Dectin-1 led to the induction of multiple proallergic (Muc5ac, Clca3, CCL17, CCL22, and IL-33) and proinflammatory (IL-1β and CXCL1) mediators that compromised lung function. Attenuated proallergic and proinflammatory responses in the absence of Dectin-1 were not associated with changes in Ido (IDO), Il12p35/Ebi3 (IL-35), IL-10, or TGF-β levels. Assessment of Th responses demonstrated that purified lung CD4(+) T cells produced IL-4, IL-13, IFN-γ, and IL-17A, but not IL-22, in a Dectin-1-dependent manner. In contrast, we observed robust, Dectin-1-dependent IL-22 production by unfractionated lung digest cells. Intriguingly, the absence of IL-22 alone mimicked the attenuated proallergic and proinflammatory responses observed in the absence of Dectin-1, suggesting that Dectin-1-mediated IL-22 production potentiated responses that led to decrements in lung function. To this end, neutralization of IL-22 improved lung function in normal mice. Collectively, these results indicate that the β-glucan receptor Dectin-1 contributes to lung inflammation and immunopathology associated with persistent fungal exposure via the production of IL-22.

Indexed as

AnimalsAspergillus fumigatusCells, CulturedChronic DiseaseDectin-1Disease Models, AnimalGlucansInterleukin-22InterleukinsLectins, C-TypeLungMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutReceptors, Immunologicbeta-glucan receptorDectin-1GlucansInterleukin-22InterleukinsLectins, C-TypeReceptors, Immunologic

Identifiers

PMID22933634
PMCPMC3448838
OpenAlexW2129837490

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.