Evidence map›Paper›PMID 18612433›Full record

ArticlePloS one2008

Galectin-4 controls intestinal inflammation by selective regulation of peripheral and mucosal T cell apoptosis and cell cycle.

Daniela Paclik, Silvio Danese, Uta Berndt, Bertram Wiedenmann, Axel Dignass, Andreas Sturm

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Methanol Extract fromAntioxidants (Basel, Switzerland) · 2025
    Article
  3. Article
  4. Review
  5. Galectin-4 potentiates CD8+ T cell immunity by enhancing MHC-I expression on dendritic cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  6. Review
  7. Review
  8. Role of Galectin-1 in the Pathogenesis of Melanoma.Journal of cancer science and clinical therapeutics · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Testicular Toxicity in Rats Exposed to AlClBiological trace element research · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Regulation of wound healing and fibrosis by galectins.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  19. Article
  20. Galectin-8, cytokines, and the storm.Biochemical Society transactions · 2022
    Review
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 3 institutions in 2 countries.

Daniela PaclikMedizinische Klinik m.S. Hepatologie und Gastroenterologie, Campus Virchow Klinikum, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Silvio Danese
Uta Berndt
Bertram Wiedenmann
Axel Dignass
Andreas Sturm
Charité - Universitätsmedizin Berlin · DEAgaplesion Markus Hospital · DEIRCCS Humanitas Research Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Galectin-4 is a carbohydrate-binding protein belonging to the galectin family. Here we provide novel evidence that galectin-4 is selectively expressed and secreted by intestinal epithelial cells and binds potently to activated peripheral and mucosal lamina propria T-cells at the CD3 epitope. The carbohydrate-dependent binding of galectin-4 at the CD3 epitope is fully functional and inhibited T cell activation, cycling and expansion. Galectin-4 induced apoptosis of activated peripheral and mucosal lamina propria T cells via calpain-, but not caspase-dependent, pathways. Providing further evidence for its important role in regulating T cell function, galectin-4 blockade by antisense oligonucleotides reduced TNF-alpha inhibitor induced T cell death. Furthermore, in T cells, galectin-4 reduced pro-inflammatory cytokine secretion including IL-17. In a model of experimental colitis, galectin-4 ameliorated mucosal inflammation, induced apoptosis of mucosal T-cells and decreased the secretion of pro-inflammatory cytokines. Our results show that galectin-4 plays a unique role in the intestine and assign a novel role of this protein in controlling intestinal inflammation by a selective induction of T cell apoptosis and cell cycle restriction. Conclusively, after defining its biological role, we propose Galectin-4 is a novel anti-inflammatory agent that could be therapeutically effective in diseases with a disturbed T cell expansion and apoptosis such as inflammatory bowel disease.

Indexed as

ApoptosisCell CycleAnimalsAntigens, CD7CalpainCD3 ComplexCell ProliferationColitisGalectin 4Inflammatory Bowel DiseasesIntegrin beta1Intestinal MucosaMiceMice, Inbred BALB CT-LymphocytesT-Lymphocyte SubsetsAntigens, CD7CalpainCD3 ComplexGalectin 4Integrin beta1

Identifiers

PMID18612433
PMCPMC2440804
OpenAlexW2089634605

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.