Evidence map›Paper›PMID 23313429›Full record

ReviewJournal of autoimmunity2013

FOXP3: genetic and epigenetic implications for autoimmunity.

Hiroto Katoh, Pan Zheng, Yang Liu

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Sex differences in disease: sex chromosome and immunity.Journal of translational medicine · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Medical research archives · 2022
    Article
  12. Article
  13. SpatiotemporalMolecular therapy. Methods & clinical development · 2021
    Article
  14. Prostaglandin E2 Reverses the Effects of DNA Methyltransferase Inhibitor and TGFB1 on the Conversion of Naive T Cells to iTregs.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2020
    Article
  15. Review
  16. Review
  17. Article
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  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

3 authors at 3 institutions in 2 countries.

Hiroto KatohDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University, Hokkaido, Japan.
Pan Zheng
Yang Liu
Children's National · USHokkaido University · JPUniversity of Michigan–Ann Arbor · US

Funding

Checkpoints of Host Response to Cellular InjuriesR01AI064350 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG, ZHENG, PAN · 2006 to 2019
$5.6M
Tumor burden and T cell immunityR01CA058033 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG · 1992 to 2013
$3.3M
FoxP3 as the X-Linked Breast Cancer Suppressor GeneR01CA120901 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG · 2007 to 2010
$1.6M
NCI NIH HHS R01 CA058033NCI NIH HHS R01 CA120901NIAID NIH HHS R01 AI064350
6 · The paper itself

Abstract

FOXP3 plays an essential role in the maintenance of self-tolerance and, thus, in preventing autoimmune diseases. Inactivating mutations of FOXP3 cause immunodysregulation, polyendocrinopathy, and enteropathy, X-linked syndrome. FOXP3-expressing regulatory T cells attenuate autoimmunity as well as immunity against cancer and infection. More recent studies demonstrated that FOXP3 is an epithelial cell-intrinsic tumor suppressor for breast, prostate, ovary and other cancers. Corresponding to its broad function, FOXP3 regulates a broad spectrum of target genes. While it is now well established that FOXP3 binds to and regulates thousands of target genes in mouse and human genomes, the fundamental mechanisms of its broad impact on gene expression remain to be established. FOXP3 is known to both activate and repress target genes by epigenetically regulating histone modifications of target promoters. In this review, we first focus on germline mutations found in the FOXP3 gene among IPEX patients, then outline possible molecular mechanisms by which FOXP3 epigenetically regulates its targets. Finally, we discuss clinical implications of the function of FOXP3 as an epigenetic modifier. Accumulating results reveal an intriguing functional convergence between FOXP3 and inhibitors of histone deacetylases. The essential epigenetic function of FOXP3 provides a foundation for experimental therapies against autoimmune diseases.

Indexed as

AutoimmunityEpigenesis, GeneticForkhead Transcription FactorsGene Expression RegulationGenetic Diseases, X-LinkedHistone DeacetylasesHumansIntestinal DiseasesMutationPolyendocrinopathies, AutoimmuneSyndromeForkhead Transcription FactorsFOXP3 protein, humanHistone Deacetylases

Identifiers

PMID23313429
PMCPMC3622774
OpenAlexW2005451808

What OpenQuestion holds

Textmetadata
LicenceTDM
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.