Evidence map›Paper›PMID 22544392›Full record

ArticleNature immunology2012

TRIM28 prevents autoinflammatory T cell development in vivo.

Shunsuke Chikuma, Naomasa Suita, Il-Mi Okazaki, Shiro Shibayama, Tasuku Honjo

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
3.7field-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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  13. The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024
    Review
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  19. Article
  20. Aging · 2020
    Article

15 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

5 authors at 3 institutions in 1 country.

Shunsuke ChikumaDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Naomasa Suita
Il-Mi Okazaki
Shiro Shibayama
Tasuku Honjo
Kyoto University · JPOno Pharmaceutical (Japan) · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRIM28 is a component of heterochromatin complexes whose function in the immune system is unknown. By studying mice with conditional T cell-specific deletion of TRIM28 (CKO mice), we found that TRIM28 was phosphorylated after stimulation via the T cell antigen receptor (TCR) and was involved in the global regulation of CD4(+) T cells. The CKO mice had a spontaneous autoimmune phenotype that was due in part to early lymphopenia associated with a defect in the production of interleukin 2 (IL-2) as well as incomplete cell-cycle progression of their T cells. In addition, CKO T cells showed derepression of the cytokine TGF-β3, which resulted in an altered cytokine balance; this caused the accumulation of autoreactive cells of the T(H)17 subset of helper T cells and of Foxp3(+) T cells. Notably, CKO Foxp3(+) T cells were unable to prevent the autoimmune phenotype in vivo. Our results show critical roles for TRIM28 in both T cell activation and T cell tolerance.

Indexed as

AnimalsAutoimmunityCD4-Positive T-LymphocytesCell CycleDNAForkhead Transcription FactorsHumansInflammationInterleukin-2Jurkat CellsMiceMice, KnockoutMice, TransgenicNuclear ProteinsOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionDNAForkhead Transcription FactorsFoxp3 protein, mouseInterleukin-2Nuclear ProteinsReceptors, Antigen, T-CellRepressor ProteinsTransforming Growth Factor beta3Trim28 protein, mouseTripartite Motif-Containing Protein 28

Identifiers

PMID22544392
OpenAlexW2137296740

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.