Evidence map›Paper›PMID 23530726›Full record

ReviewBritish journal of pharmacology2013

IL-22 in tissue-protective therapy.

Heiko Mühl, Patrick Scheiermann, Malte Bachmann, Lorena Härdle, Anika Heinrichs, Josef Pfeilschifter

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  9. Article
  10. The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Interleukin-22: a potential therapeutic target in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Heiko Mühlpharmazentrum frankfurt/ZAFES, University Hospital, Goethe University Frankfurt, Frankfurt am Main, Germany. h.muehl@em.uni-frankfurt.de
Patrick Scheiermann
Malte Bachmann
Lorena Härdle
Anika Heinrichs
Josef Pfeilschifter
Goethe University Frankfurt · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-22, a member of the IL-10 cytokine family, has recently gained significant attention as a protective agent in murine models of diseases driven by epithelial injury. Like its biochemical and functional sibling IL-10, IL-22 elicits cellular activation primarily by engaging the STAT3 signalling pathway. Exclusively produced by leukocytes, but targeting mostly cells of epithelial origin, IL-22 has been proposed as a specialized cytokine messenger acting between leukocytic and non-leukocytic cell compartments. A lack of response in leukocytes to IL-22 mirrors tightly controlled IL-22 receptor expression and probably explains the apparent lack of instant adverse effects after systemic IL-22 administration to mice. Anti-apoptotic, pro-proliferative and pro-regenerative characteristics the major biological properties of this cytokine. Specifically, application of IL-22 is associated with tissue protection and/or regeneration in murine models of infection/microbe-driven inflammation at host/environment interfaces, ventilator-induced lung injury, pancreatitis and liver damage. Overall, preclinical studies would support therapeutic administration of seemingly well-tolerated recombinant IL-22 for treatment of an array of acute diseases manifested in epithelial tissues. However, the feasibility of prolonged administration of this cytokine is expected to be restricted by the tumourigenic potential of the IL-22/STAT3 axis. IL-22, moreover, apparently displays an inherent context-specific capacity to amplify distinct aspects of autoimmune inflammation. Here, the prospects, expectations and restrictions of IL-22 administration in tissue-protective therapy are discussed.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalApoptosisCell ProliferationDisease Models, AnimalDrugs, InvestigationalHepatic Stellate CellsHumansInterleukin-22InterleukinsMAP Kinase Signaling SystemMucous MembraneProtective AgentsReceptors, InterleukinRecombinant ProteinsRegenerationAnti-Inflammatory Agents, Non-SteroidalDrugs, InvestigationalInterleukin-22interleukin-22 receptorInterleukinsProtective AgentsReceptors, InterleukinRecombinant ProteinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID23530726
PMCPMC3687657
OpenAlexW1926103424

What OpenQuestion holds

Textmetadata
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.