Evidence map›Paper›PMID 21798734›Full record

ReviewCurrent opinion in immunology2011

Histone/protein deacetylases control Foxp3 expression and the heat shock response of T-regulatory cells.

Ulf H Beier, Tatiana Akimova, Yujie Liu, Liqing Wang, Wayne W Hancock

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
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

59 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
  2. CD38 endows local antigen-specific TNature immunology · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Insights into the therapeutic potential of histone deacetylase inhibitor/immunotherapy combination regimens in solid tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  10. Article
  11. SIRT1: A promising therapeutic target for chronic pain.CNS neuroscience & therapeutics · 2022
    Review
  12. Review
  13. Valproic Acid Inhibits Glioma and Its Mechanisms.Journal of healthcare engineering · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. FoxP3 in TClinical and experimental immunology · 2020
    Review
  18. Review
  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

5 authors at 2 institutions in 1 country.

Ulf H BeierDivision of Nephrology, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, USA.
Tatiana Akimova
Yujie Liu
Liqing Wang
Wayne W Hancock
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Transgenic and mutant animalP01AI073489 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI KATSUMATA, MAKOTO · 2008 to 2012
$7.1M
Targeting Sirtuin-1 to enhance Foxp3+ regulatory T-cell functionK08AI095353 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI BEIER, ULF · 2011 to 2015
$650k
NIAID NIH HHS AI073489NIAID NIH HHS K08 AI095353NIAID NIH HHS K08AI095353NIAID NIH HHS P01 AI073489
6 · The paper itself

Abstract

Lysine ɛ-acetylation is a post-translational modification that alters the biochemical properties of many proteins. The reaction is catalyzed by histone/protein acetyltransferases (HATs), and is reversed by histone/protein deacetylases (HDACs). As a result, HATs and HDACs constitute an important, though little recognized, set of proteins that control the functions of T-regulatory (Treg) cells. Targeting certain HDACs, especially HDAC6, HDAC9, and Sirtuin-1 (Sirt1), can augment Treg suppressive potency by several distinct and potentially additive mechanisms. These involve promoting Forkhead box p3 (Foxp3) gene expression and preserving Foxp3 lysine ɛ-acetylation, which infers resistance to ubiquitination and proteasomal degradation, and increases DNA binding. Moreover, depleting certain HDAC can enhance the heat shock response, which increases the tenacity of Treg to survive under stress, and helps preserve a suppressive phenotype. As a result, HDAC inhibitor therapy can be used to enhance Treg functions in vivo and have beneficial effects on allograft survival and autoimmune diseases.

Indexed as

Adaptive ImmunityOrgan TransplantationAcetylationAnimalsAutoimmune DiseasesForkhead Transcription FactorsGene Expression RegulationGraft RejectionHeat-Shock ResponseHistone AcetyltransferasesHistone Deacetylase InhibitorsHistone DeacetylasesHumansMiceProtein Processing, Post-TranslationalT-Lymphocytes, RegulatoryForkhead Transcription FactorsFOXP3 protein, humanFoxp3 protein, mouseHistone AcetyltransferasesHistone Deacetylase InhibitorsHistone Deacetylases

Identifiers

PMID21798734
PMCPMC3190028
OpenAlexW2057868230

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.