Evidence map›Paper›PMID 26604637›Full record

ReviewWorld journal of gastroenterology2015

Th17 plasticity and its changes associated with inflammatory bowel disease.

Aito Ueno, Abhisek Ghosh, Daniel Hung, Ji Li, Humberto Jijon

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
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  5. Dissecting PGENature communications · 2026
    Article
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  7. Review
  8. Article
  9. Review
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  15. Molecules (Basel, Switzerland) · 2023
    Article
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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

5 authors at 1 institution in 1 country.

Aito UenoAito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada.
Abhisek GhoshAito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada.
Daniel HungAito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada.
Ji LiAito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada.
Humberto JijonAito Ueno, Daniel Hung, Humberto Jijon, Department of Medicine, University of Calgary, Calgary T2N 1N4, Alberta, Canada.
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4 T helper (Th) cell differentiation into distinct T cell subsets is critical to the normal function of the immune system. Until recently, the paradigm held that naïve T cells differentiated into distinct subsets under the guidance of environmental cues (e.g., cytokines) and that once polarized, these cells were committed to a particular functional state. However, the existence of transdifferentiated T cell populations, which express signature transcription factors and cytokines associated with more than one Th subset, challenges the immutability of T helper subsets and suggests that plasticity is a feature of multifaceted immune responses. How this process impacts immune dysregulation in diseases such as inflammatory bowel diseases (IBD) and the machinery that underlies this process is far from fully understood. Interleukin (IL)-17 secreting helper T (Th17) cells have been heavily implicated in tissue-specific immune pathology including murine models of IBD, human Crohn's disease and ulcerative colitis. Plasticity within this subset is suggested by the existence of IL-17 secreting cells, which, can also secrete interferon-γ, the signature cytokine for Th1 cells or, can co-express the anti-inflammatory transcription factor forkhead box p3, a signature transcription factor of regulatory T cells. In this review we mainly discuss evidence for Th17 plasticity, mechanisms, which govern it, and highlight the potential to therapeutically target this process in human IBD.

Indexed as

Cell PlasticityAnimalsCell CommunicationCellular MicroenvironmentColonCytokinesHumansInflammation MediatorsInflammatory Bowel DiseasesPhenotypeSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryCytokinesInflammation MediatorsInflammatory bowel diseaseRegulatory T cellsT cell plasticityTh7

Identifiers

PMID26604637
PMCPMC4649113
OpenAlexW2410151108

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.