Evidence map›Paper›PMID 29245178›Full record

ReviewArthritis & rheumatology (Hoboken, N.J.)2018

Review: Transcriptional Regulation of CD4+ T Cell Differentiation in Experimentally Induced Arthritis and Rheumatoid Arthritis.

Yuya Kondo, Masahiro Yokosawa, Shunta Kaneko, Kotona Furuyama, Seiji Segawa, Hiroto Tsuboi, Isao Matsumoto, Takayuki Sumida

Open access · hybridAbstract readReview
In one paragraph

Review in Arthritis & rheumatology (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  3. Article
  4. Article
  5. Dysfunctional glycolysis-UCP2-fatty acid oxidation promotes CTLA4Molecular medicine (Cambridge, Mass.) · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Endoplasmic reticulum aminopeptidase 2 regulates CD4Arthritis research & therapy · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Yuya KondoUniversity of Tsukuba, Tsukuba, Japan.
Masahiro YokosawaUniversity of Tsukuba, Tsukuba, Japan.
Shunta KanekoUniversity of Tsukuba, Tsukuba, Japan.
Kotona FuruyamaUniversity of Tsukuba, Tsukuba, Japan.
Seiji SegawaUniversity of Tsukuba, Tsukuba, Japan.
Hiroto TsuboiUniversity of Tsukuba, Tsukuba, Japan.
Isao MatsumotoUniversity of Tsukuba, Tsukuba, Japan.
Takayuki SumidaUniversity of Tsukuba, Tsukuba, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of the joint synovium and infiltration by activated inflammatory cells. CD4+ T cells form a large proportion of the inflammatory cells invading the synovial tissue, and are involved in the RA pathologic process. In general, CD4+ T cells differentiate into various T helper cell subsets and acquire the functional properties to respond to specific pathogens, and also mediate some autoimmune disorders such as RA. Because the differentiation of T helper cell subsets is determined by the expression of specific transcription factors in response to the cytokine environment, these transcription factors are considered to have a role in the pathology of RA. Treg cells control an excess of T cell-mediated immune response, and the transcription factor FoxP3 is critical for the differentiation and function of Treg cells. Treg cell dysfunction can result in the development of systemic autoimmunity. In this review, we summarize how the expression of transcription factors modulates T helper cell immune responses and the development of autoimmune diseases, especially in RA. Understanding the role of transcription factors in the pathogenesis of autoimmunity may lead to novel therapeutic strategies to control the differentiation and function of both T helper cells and Treg cells.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAutoimmune DiseasesCD4-Positive T-LymphocytesCell DifferentiationHumansRegulatory Elements, TranscriptionalT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryTranscription, Genetic

Identifiers

PMID29245178
PMCPMC5947164
OpenAlexW2771930301

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.