Evidence map›Paper›PMID 33433611›Full record

ArticleThe Journal of experimental medicine2021

The Cxxc1 subunit of the Trithorax complex directs epigenetic licensing of CD4+ T cell differentiation.

Masahiro Kiuchi, Atsushi Onodera, Kota Kokubo, Tomomi Ichikawa, Yuki Morimoto, Eiryo Kawakami, Naoya Takayama, Koji Eto, Haruhiko Koseki, Kiyoshi Hirahara and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. A multi-omics analysis of human fibroblasts overexpressing anbioRxiv : the preprint server for biology · 2025
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  8. The USP7-STAT3-granzyme-Par-1 axis regulates allergic inflammation by promoting differentiation of IL-5-producing Th2 cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

11 authors at 1 institution in 1 country.

Masahiro Kiuchi *Department of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Atsushi Onodera *Department of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Kota KokuboDepartment of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Tomomi IchikawaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Yuki MorimotoDepartment of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Eiryo KawakamiArtificial Intelligence Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Naoya TakayamaDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Koji EtoDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Haruhiko KosekiDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kiyoshi HiraharaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different dynamics of gene expression are observed during cell differentiation. In T cells, genes that are turned on early or turned off and stay off have been thoroughly studied. However, genes that are initially turned off but then turned on again after stimulation has ceased have not been defined; they are obviously important, especially in the context of acute versus chronic inflammation. Using the Th1/Th2 differentiation paradigm, we found that the Cxxc1 subunit of the Trithorax complex directs transcription of genes initially down-regulated by TCR stimulation but up-regulated again in a later phase. The late up-regulation of these genes was impaired either by prolonged TCR stimulation or Cxxc1 deficiency, which led to decreased expression of Trib3 and Klf2 in Th1 and Th2 cells, respectively. Loss of Cxxc1 resulted in enhanced pathogenicity in allergic airway inflammation in vivo. Thus, Cxxc1 plays essential roles in the establishment of a proper CD4+ T cell immune system via epigenetic control of a specific set of genes.

Indexed as

Epigenesis, GeneticAnimalsCD4-Positive T-LymphocytesCell Cycle ProteinsCell DifferentiationDisease Models, AnimalDown-RegulationFemaleHistone-Lysine N-MethyltransferaseKruppel-Like Transcription FactorsMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-CellRespiratory HypersensitivitySignal TransductionCell Cycle ProteinsCxxc1 protein, mouseHistone-Lysine N-MethyltransferaseKlf2 protein, mouseKruppel-Like Transcription FactorsReceptors, Antigen, T-CellTrans-ActivatorsTRB3 protein, mouse

Identifiers

PMID33433611
PMCPMC7808308
OpenAlexW3121111775

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.