Evidence map›Paper›PMID 22359410›Full record

ReviewInflammatory bowel diseases2012

Healing of intestinal inflammation by IL-22.

Atsushi Mizoguchi

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammatory bowel diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. AhR ligands fromJournal of virology · 2024
    Article
  9. IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Th22 cells and the intestinal mucosal barrier.Frontiers in immunology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

17 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

1 author at 1 institution in 1 country.

Atsushi MizoguchiMolecular Pathology Unit, Massachusetts General Hospital and Department of Pathology, Harvard Medical School, Charlestown, Massachusetts, USA. amizoguchi@partners.org
Massachusetts General Hospital · US

Funding

Inducible Regulatory B cells IBREGR01AI081807 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI REINECKER, HANS-CHRISTIAN · 2011 to 2015
$1.9M
Endoscopic Theranostics SystemRC1DK086242 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MIZOGUCHI, ATSUSHI, YUN, SEOK-HYUN ANDY · 2009 to 2010
$965k
NIAID NIH HHS R01 AI081807NIDDK NIH HHS RC1 DK086242NIDDK NIH HHS RC1DK086242
6 · The paper itself

Abstract

An interleukin (IL)-10 family cytokine, IL-22 is characterized by several unique biological properties, including 1) the target restricted to innate cells; 2) the distinct expression pattern between large and small intestines; 3) alteration of the cellular source depending on several factors; 4) the dual abilities to serve as protective versus proinflammatory mediators in inflammatory responses; and 5) the close association with some major inflammatory bowel disease (IBD) susceptibility genes. The major functions of IL-22 in the intestine are the stimulation of epithelial cells to produce a wide variety of antibacterial proteins, the reinforcement of mucus barrier through stimulation of mucin 1 production under intestinal inflammatory conditions, and the enhancement of epithelial regeneration with goblet cell restitution. Through these beneficial functions, IL-22 contributes to the improvement of some types of experimental chronic colitis, which are mediated by T helper (Th)1 or Th2 responses. Most important, studies using both loss-of-function and gain-of-function approaches have clearly demonstrated the ability of IL-22 to promote intestinal wound healing from acute intestinal injury. These findings highlight IL-22 as an attractive and promising target for future IBD therapy. Alternatively, the enormous progress in the field of IL-22 biology has also suggested more complicated mechanisms with the IL-22 pathway than previously predicted. This review article briefly summarizes previous and current knowledge on IL-22 particularly associated with intestinal inflammation.

Indexed as

AnimalsHumansInflammationInterleukin-22InterleukinsIntestinesInterleukin-22Interleukins

Identifiers

PMID22359410
PMCPMC3366176
OpenAlexW2062262876

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.