Evidence map›Paper›PMID 23022954›Full record

ArticleGastroenterology2012

Aryl hydrocarbon receptor regulates pancreatic IL-22 production and protects mice from acute pancreatitis.

Jing Xue, David T C Nguyen, Aida Habtezion

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  6. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  7. The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  8. The TRIM28/miR133a/CD47 axis acts as a potential therapeutic target in pancreatic necrosis by impairing efferocytosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  9. Article
  10. The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  11. Article
  12. Review
  13. Review
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  15. Article
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10 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

3 authors at 1 institution in 1 country.

Jing XueStanford University School of Medicine, Department of Medicine, Division of Gastroenterology and Hepatology, Stanford, California, USA.
David T C Nguyen
Aida Habtezion
Stanford University · US

Funding

Proteomics/GenomicsP30DK056339 · NIDDK · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2001 to 2010
$10.4M
Role of hemeoxygenase-1 in experimental acute pancreatitisR01DK092421 · NIDDK · STANFORD UNIVERSITY · PI HABTEZION, AIDA · 2011 to 2020
$3.5M
NIDDK NIH HHS DK56339NIDDK NIH HHS P30 DK056339NIDDK NIH HHS R01 DK092421
6 · The paper itself

Abstract

BACKGROUND &

aimsThe type of immune response during development of acute pancreatitis (AP) determines disease severity. Pancreatic epithelial cells express the interleukin (IL)-22 receptor A1 (IL-22RA1). The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that regulates expression of IL-22. We investigated sources and role of IL-22 in the pancreas, along with the effects of AhR activation on IL-22 expression and AP progression in mice.

methodsWe analyzed the effects of recombinant IL-22, a monoclonal antibody against IL-22, and agonists and antagonists of AhR in mice with AP (induced with caerulein or a choline-deficient diet supplemented with DL-ethionine) and control mice. We also analyzed transgenic mice with AhR deficiency (AhR(d) and AhR(-/-) mice).

resultsCD4(+) T cells were the main source of IL-22 in pancreatic tissues from healthy mice. During development of AP, numbers of IL-22(+) CD4(+) T cells were reduced, whereas IL-22RA1 was up-regulated. Consistent with high levels of IL-22RA1 expression, pancreatic acinar cells responded to IL-22 signaling via signal transducers and activators of transcription 3; administration of IL-22 reduced AP and associated lung injury in mice. AhR was required for production of IL-22 and protected mice from AP. Mice that did not respond to AhR activation developed AP, but administration of IL-22 reduced AP; blockade of IL-22 reversed the ability of activated AhR to protect against AP.

conclusionsAhR activation protects mice from AP by inducing expression of IL-22. AhR therefore mediates interactions between pancreatic leukocytes and epithelial cells and might be developed as a therapeutic target.

Indexed as

Acute DiseaseAnimalsCD4-Positive T-LymphocytesCeruletideCholine DeficiencyDisease Models, AnimalFemaleInterleukin-22InterleukinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicPancreasPancreatitisCeruletideInterleukin-22InterleukinsReceptors, Aryl HydrocarbonSTAT3 Transcription Factor

Identifiers

PMID23022954
PMCPMC3647696
OpenAlexW2027997166

What OpenQuestion holds

Textmetadata
LicenceTDM
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.