Evidence map›Paper›PMID 28287113›Full record

ArticleCellular & molecular immunology2018

Loss of T-cell protein tyrosine phosphatase in the intestinal epithelium promotes local inflammation by increasing colonic stem cell proliferation.

Stéphanie Bussières-Marmen, Valérie Vinette, Jeremy Gungabeesoon, Isabelle Aubry, Luis Alberto Pérez-Quintero, Michel L Tremblay

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025
    Review
  5. Article
  6. Inflammation in glomerular diseases.Frontiers in immunology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. TRIM18-Regulated STAT3 Signaling PathwayFrontiers in physiology · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling.International journal of molecular sciences · 2018
    Review
  17. Article
  18. 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.

Stéphanie Bussières-MarmenDepartment of Biochemistry, McGill University, Montréal, Québec, Canada.
Valérie VinetteDepartment of Biochemistry, McGill University, Montréal, Québec, Canada.
Jeremy GungabeesoonDepartment of Microbiology and Immunology, McGill University, Montréal, Québec, Canada.
Isabelle AubryRosalind and Morris Goodman Cancer Research Centre, Montréal, Québec, Canada.
Luis Alberto Pérez-QuinteroDepartment of Biochemistry, McGill University, Montréal, Québec, Canada.
Michel L TremblayDepartment of Biochemistry, McGill University, Montréal, Québec, Canada. michel.tremblay@mcgill.ca.
McGill University · CAOccupational Cancer Research Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell protein tyrosine phosphatase (TC-PTP) has a critical role in the development of the immune system and has been identified as a negative regulator of inflammation. Single-nucleotide polymorphisms in the TC-PTP locus have been associated with increased susceptibility to inflammatory bowel diseases (IBDs) in patients. To further understand how TC-PTP is related to IBDs, we investigated the role of TC-PTP in maintaining the intestinal epithelial barrier using an in vivo genetic approach. Intestinal epithelial cell (IEC)-specific deletion of TC-PTP was achieved in a mouse model at steady state and in the context of dextran sulphate sodium (DSS)-induced colitis. Knockout (KO) of TC-PTP in IECs did not result in an altered intestinal barrier. However, upon DSS treatment, IEC-specific TC-PTP KO mice displayed a more severe colitis phenotype with a corresponding increase in the immune response and inflammatory cytokine profile. The absence of TC-PTP caused an altered turnover of IECs, which is further explained by the role of the tyrosine phosphatase in colonic stem cell (CoSC) proliferation. Our results suggest a novel role for TC-PTP in regulating the homeostasis of CoSC proliferation. This supports the protective function of TC-PTP against IBDs, independently of its previously demonstrated role in intestinal immunity.

Indexed as

AnimalsCell ProliferationColitisColonCytokinesDextran SulfateDisease SusceptibilityEnterocytesHomeostasisInflammationIntestinal MucosaMice, Inbred C57BLMice, KnockoutNeutrophilsProtein Tyrosine Phosphatase, Non-Receptor Type 2Stem CellsCytokinesDextran SulfateProtein Tyrosine Phosphatase, Non-Receptor Type 2Colonic stem cellsDSS-induced colitisintestinal epithelial barrierTC-PTP

Identifiers

PMID28287113
PMCPMC6052838
OpenAlexW2596957207

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.