Evidence map›Paper›PMID 28811323›Full record

ArticleThe Journal of experimental medicine2017

IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite-induced asthma models.

Takashi Ito, Koichi Hirose, Aiko Saku, Kenta Kono, Hiroaki Takatori, Tomohiro Tamachi, Yoshiyuki Goto, Jean-Christophe Renauld, Hiroshi Kiyono, Hiroshi Nakajima

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

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  10. Characteristics ofFrontiers in immunology · 2025
    Article
  11. Article
  12. IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024
    Review
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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

10 authors at 2 institutions in 2 countries.

Takashi ItoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Koichi HiroseDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan hirose-kh@faculty.chiba-u.jp.ORCID http://orcid.org/0000-0001-7498-9630
Aiko SakuDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kenta KonoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID http://orcid.org/0000-0003-4167-4549
Hiroaki TakatoriDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomohiro TamachiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yoshiyuki GotoDivision of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Jean-Christophe RenauldLudwig Institute for Cancer Research, Brussels Branch, Brussels, Belgium.ORCID http://orcid.org/0000-0003-1736-2131
Hiroshi KiyonoDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hiroshi NakajimaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan nakajimh@faculty.chiba-u.jp.
Chiba University · JPLudwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that IL-22, one of the Th17 cell-related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.

Indexed as

AnimalsAsthmaDisease Models, AnimalHypersensitivityInterleukin-22InterleukinsMiceMice, Inbred C57BLMice, KnockoutPancreatitis-Associated ProteinsProteinsPyroglyphidaeTh17 CellsTh2 CellsInterleukin-22InterleukinsPancreatitis-Associated ProteinsProteinsReg3g protein, mouse

Identifiers

PMID28811323
PMCPMC5626396
OpenAlexW2749158100

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.