Evidence map›Paper›PMID 36769019›Full record

ReviewInternational journal of molecular sciences2023

CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.

Raquel Gomez-Bris, Angela Saez, Beatriz Herrero-Fernandez, Cristina Rius, Hector Sanchez-Martinez, Jose M Gonzalez-Granado

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

147 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. CD4Sensors (Basel, Switzerland) · 2026
    Pooled it
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  4. Pooled it
  5. Trial
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  8. Review
  9. Article
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  12. Review
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  15. Journal of bacteriology · 2026
    Review
  16. Article
  17. Article
  18. Branched-chain amino acids ameliorate CD4NPJ Parkinson's disease · 2026
    Article
  19. Article
  20. Review

87 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

6 authors.

Raquel Gomez-BrisLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0001-6665-7732
Angela SaezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0002-9189-4737
Beatriz Herrero-FernandezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.
Cristina RiusDepartment of History of Science and Information Science, School of Medicine and Dentistry, University of Valencia, 46010 Valencia, Spain.ORCID 0000-0002-0572-5620
Hector Sanchez-MartinezLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.
Jose M Gonzalez-GranadoLamImSys Lab, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28041 Madrid, Spain.ORCID 0000-0002-1177-869X

Funding

Comunidad de Madrid PEJ-2020-TL/BMD-17604Instituto de Salud Carlos III PI20/00306Ministerio de Ciencia, Innovación y Universidades (MCNU) FPU19/01774Ministerio de Ciencia, Innovación y Universidades (MCNU), FPU18/00895
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is an umbrella term for the chronic immune-mediated idiopathic inflammation of the gastrointestinal tract, manifesting as Crohn's disease (CD) or ulcerative colitis (UC). IBD is characterized by exacerbated innate and adaptive immunity in the gut in association with microbiota dysbiosis and the disruption of the intestinal barrier, resulting in increased bacterial exposure. In response to signals from microorganisms and damaged tissue, innate immune cells produce inflammatory cytokines and factors that stimulate T and B cells of the adaptive immune system, and a prominent characteristic of IBD patients is the accumulation of inflammatory T-cells and their proinflammatory-associated cytokines in intestinal tissue. Upon antigen recognition and activation, CD4 T-cells differentiate towards a range of distinct phenotypes: T helper(h)1, Th2, Th9, Th17, Th22, T follicular helper (Tfh), and several types of T-regulatory cells (Treg). T-cells are generated according to and adapt to microenvironmental conditions and participate in a complex network of interactions among other immune cells that modulate the further progression of IBD. This review examines the role of the CD4 T-cells most relevant to IBD, highlighting how these cells adapt to the environment and interact with other cell populations to promote or inhibit the development of IBD.

Indexed as

CD4-Positive T-LymphocytesInflammatory Bowel DiseasesCytokinesHumansInflammationIntestinal MucosaT-Lymphocyte SubsetsCytokinesadaptive immune systemCrohn’s diseaseinflammatory bowel diseaseregulatory T-cellTh1Th17Th19Th2Th22Tregulcerative colitis

Identifiers

PMID36769019
PMCPMC9916759

What Socratic 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 Socratic graph.