Evidence map›Paper›PMID 31125332›Full record

ArticlePLoS biology2019

Foxp1 is critical for the maintenance of regulatory T-cell homeostasis and suppressive function.

Jiazi Ren, Lei Han, Jinyi Tang, Yuanhua Liu, Xiaoxue Deng, Qiuyue Liu, Pei Hao, Xiaoming Feng, Bin Li, Hui Hu and 1 more

Abstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Engineered Foxp1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  9. Article
  10. Observational
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Journal of pediatric genetics · 2024
    Article
  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

11 authors.

Jiazi RenCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Lei HanCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Jinyi TangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Yuanhua LiuCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Xiaoxue DengCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Qiuyue LiuCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Pei HaoCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Xiaoming FengState Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Bin LiShanghai Institute of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Hui HuDepartment of Microbiology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Haikun WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-4714-4672

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Transcriptional regulation of T cell quiescience and activationR01AI095439 · NIAID · WISTAR INSTITUTE · PI HU, HUI · 2012 to 2016
$1.9M
Negative regulatory pathways in T cell quiescence and T cell responseR01AI103162 · NIAID · WISTAR INSTITUTE · PI HU, HUI · 2012 to 2016
$1.2M
NCI NIH HHS P30 CA013148NIAID NIH HHS R01 AI095439NIAID NIH HHS R01 AI103162
6 · The paper itself

Abstract

Regulatory T (Treg) cells play central roles in maintaining immune homeostasis and self-tolerance. However, the molecular mechanisms underlying Treg cell homeostasis and suppressive function are still not fully understood. Here, we report that the deletion of another P subfamily members of the forkhead box (Foxp) subfamily member Foxp1 in Treg cells led to increased numbers of activated Treg (aTreg) cells at the expense of quiescent Treg cells, and also resulted in impaired Treg suppressive function. Mice with Foxp1-deficient Treg cells developed spontaneous inflammatory disease with age; they also had more severe inflammatory disease in colitis and experimental autoimmune encephalomyelitis (EAE) models. Mechanistically, we found that Foxp1 bound to the conserved noncoding sequence 2 (CNS2) element of the Foxp3 locus and helped maintain Treg suppressive function by stabilizing the Foxp3 expression. Furthermore, we found that Foxp1 and Foxp3 coordinated the regulation of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression levels. Taken together, our study demonstrates that Foxp1 plays critical roles in both maintaining Treg cell quiescence during homeostasis and regulating Treg suppressive function.

Indexed as

HomeostasisAnimalsCell DifferentiationCTLA-4 AntigenForkhead Transcription FactorsHEK293 CellsHumansLymphocyte ActivationMice, TransgenicRepressor ProteinsT-Lymphocytes, RegulatoryTranscription, GeneticCTLA-4 AntigenCTLA4 protein, humanForkhead Transcription FactorsFoxp1 protein, mouseFoxp3 protein, mouseRepressor Proteins

Identifiers

PMID31125332
PMCPMC6534289

What OpenQuestion holds

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LicenceCC BY
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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.