Evidence map›Paper›PMID 29651155›Full record

ArticleNature communications2018

Epigenetic activation during T helper 17 cell differentiation is mediated by Tripartite motif containing 28.

Yu Jiang, Ying Liu, Huiping Lu, Shao-Cong Sun, Wei Jin, Xiaohu Wang, Chen Dong

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Yu JiangInstitute for Immunology and School of Medicine, Tsinghua University, 100084, Beijing, China.
Ying LiuDepartment of Medicine, Division of Regenerative Medicine, Ansary Stem Cell Institute, Weill Cornell Medical College, 1300 York Avenue, New York, NY, 10065, USA.
Huiping LuInstitute for Immunology and School of Medicine, Tsinghua University, 100084, Beijing, China.
Shao-Cong SunDepartment of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX, 77030, USA.
Wei JinInstitute for Immunology and School of Medicine, Tsinghua University, 100084, Beijing, China.
Xiaohu WangInstitute for Immunology and School of Medicine, Tsinghua University, 100084, Beijing, China.
Chen DongInstitute for Immunology and School of Medicine, Tsinghua University, 100084, Beijing, China. chendong@tsinghua.edu.cn.ORCID http://orcid.org/0000-0002-0084-9130
Tsinghua University · CNCornell University · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulation is important for T-cell fate decision. Although STAT3 is known to initiate Th17 differentiation program, the downstream mechanism is unclear. Here we show that Tripartite motif containing 28 (Trim28) expression in Th17 cells is required for Th17-mediated cytokine production and experimental autoimmune diseases. Genome-wide occupancy analysis reveals that TRIM28-bound regions overlap with almost all Th17-specific super-enhancers (SE), and that those SEs are impaired by the deficiency of STAT3 or TRIM28, but not of RORγt. Importantly, IL-6-STAT3 signaling facilitates TRIM28 binding to the Il17-Il17f locus, and this process is required for epigenetic activation and high-order chromosomal interaction. TRIM28 also forms a complex with STAT3 and RORγt, and promotes the recruitment of RORγt to its target cytokine genes. Our study thus suggests TRIM28 to be important for the epigenetic activation during Th17 cell differentiation, and prompts the potential use of epigenetic interventions for Th17-related autoimmune diseases.

Indexed as

Epigenesis, GeneticAnimalsCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalEnhancer Elements, GeneticGenome-Wide Association StudyHematopoiesisInterleukin-17Interleukin-6Lymphocyte ActivationMiceMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 3Protein BindingSignal TransductionSTAT3 Transcription FactorInterleukin-17Interleukin-6interleukin-6, mouseNuclear Receptor Subfamily 1, Group F, Member 3Stat3 protein, mouseSTAT3 Transcription FactorTrim28 protein, mouseTripartite Motif-Containing Protein 28

Identifiers

PMID29651155
PMCPMC5897371
OpenAlexW2797910264

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.