Evidence map›Paper›PMID 30071700›Full record

ReviewInternational journal of molecular sciences2018

Reevaluation of Pluripotent Cytokine TGF-β3 in Immunity.

Toshihiko Komai, Tomohisa Okamura, Mariko Inoue, Kazuhiko Yamamoto, Keishi Fujio

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Peritendinous adhesion: Therapeutic targets and progress of drug therapy.Computational and structural biotechnology journal · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. The Role of TGF-β3 in Radiation Response.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 2 institutions in 1 country.

Toshihiko KomaiDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. tkomai-hok@umin.ac.jp.ORCID 0000-0001-5890-3606
Tomohisa OkamuraDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. tomohisa-tky@umin.ac.jp.
Mariko InoueDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. mariinoue-tky@umin.ac.jp.ORCID 0000-0002-2482-7753
Kazuhiko YamamotoDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. kazuhiko.yamamoto@riken.jp.
Keishi FujioDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan. kfujio-tky@umin.ac.jp.
The University of Tokyo · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-βs are pluripotent cytokines with stimulatory and inhibitory properties for multiple types of immune cells. Analyses of genetic knockouts of each isoform of TGF-β have revealed differing expression patterns and distinct roles for the three mammalian isoforms of TGF-β. Considerable effort has been focused on understanding the molecular mechanisms of TGF-β1-mediated immune regulation, given its pivotal role in prohibiting systemic autoimmune disease. In recent years, functional similarities and differences between the TGF-β isoforms have delineated their distinct roles in the development of immunopathology and immune tolerance, with increased recent attention being focused on TGF-β3. In addition to the characteristic properties of each TGF-β isoform, recent progress has identified determinants of context-dependent functionality, including various cellular targets, cytokine concentrations, tissue microenvironments, and cytokine synergy, which combine to shape the physiological and pathophysiological roles of the TGF-βs in immunity. Controlling TGF-β production and signaling is being tested as a novel therapeutic strategy in multiple clinical trials for several human diseases. This review highlights advances in the understanding of the cellular sources, activation processes, contextual determinants, and immunological roles of TGF-β3 with comparisons to other TGF-β isoforms.

Indexed as

AnimalsAutoimmune DiseasesHumansProtein IsoformsSignal TransductionTransforming Growth Factor beta3Protein IsoformsTGFB3 protein, humanTransforming Growth Factor beta3autoimmune diseasefibrosisimmune toleranceimmunometabolismregulatory T celltransforming growth factor-β1transforming growth factor-β3

Identifiers

PMID30071700
PMCPMC6121403
OpenAlexW2887387679

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.