Evidence map›Paper›PMID 28819166›Full record

ArticleScientific reports2017

Histone/protein deacetylase 11 targeting promotes Foxp3+ Treg function.

Jianbing Huang, Liqing Wang, Satinder Dahiya, Ulf H Beier, Rongxiang Han, Arabinda Samanta, Joel Bergman, Eduardo M Sotomayor, Edward Seto, Alan P Kozikowski and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
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  7. HDAC11 Regulates RNA Splicing via De-Fatty Acylation of SF3B2.bioRxiv : the preprint server for biology · 2026
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  18. Emerging role of HDAC11 in skeletal muscle biology.Frontiers in cell and developmental biology · 2024
    Article
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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 5 institutions in 2 countries.

Jianbing HuangDepartment of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Liqing WangDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Satinder DahiyaDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Ulf H BeierDivision of Nephrology, Department of Pediatrics, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Rongxiang HanDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Arabinda SamantaDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Joel BergmanDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Eduardo M SotomayorGeorge Washington University Cancer Center, Washington, DC, 20037, USA.
Edward SetoGeorge Washington University Cancer Center, Washington, DC, 20037, USA.
Alan P KozikowskiDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, 60612, USA.
Wayne W HancockDivision of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Diseases, Children's Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA. whancock@mail.med.upenn.edu.
University of Pennsylvania · USChildren's Hospital of Philadelphia · USGeorge Washington University · USUniversity of Illinois Chicago · USXinHua Hospital · CN

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
ANTI-INFLAMMATORY EFFECTS OF TARGETING THE HDAC6/HSP90 PATHWAYR56AI095276 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI HANCOCK, WAYNE WILLIAM · 2011 to 2011
$209k
NIAID NIH HHS K08 AI095353NIAID NIH HHS P01 AI073489NIAID NIH HHS R56 AI095276
6 · The paper itself

Abstract

Current interest in Foxp3+ T-regulatory (Treg) cells as therapeutic targets in transplantation is largely focused on their harvesting pre-transplant, expansion and infusion post-transplantation. An alternate strategy of pharmacologic modulation of Treg function using histone/protein deacetylase inhibitors (HDACi) may allow more titratable and longer-term dosing. However, the effects of broadly acting HDACi vary, such that HDAC isoform-selective targeting is likely required. We report data from mice with constitutive or conditional deletion of HDAC11 within Foxp3+ Treg cells, and their use, along with small molecule HDAC11 inhibitors, in allograft models. Global HDAC11 deletion had no effect on health or development, and compared to WT controls, Foxp3+ Tregs lacking HDAC11 showed increased suppressive function, and increased expression of Foxp3 and TGF-β. Likewise, compared to WT recipients, conditional deletion of HDAC11 within Tregs led to long-term survival of fully MHC-mismatched cardiac allografts, and prevented development of transplant arteriosclerosis in an MHC class II-mismatched allograft model. The translational significance of HDAC11 targeting was shown by the ability of an HDAC11i to promote long-term allograft allografts in fully MHC-disparate strains. These data are powerful stimuli for the further development and testing of HDAC11-selective pharmacologic inhibitors, and may ultimately provide new therapies for transplantation and autoimmune diseases.

Indexed as

AllograftsAnimalsForkhead Transcription FactorsGene Expression ProfilingGraft SurvivalHeart TransplantationHEK293 CellsHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansMaleMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicForkhead Transcription FactorsFoxp3 protein, mouseHdac11 protein, mouseHistone Deacetylase InhibitorsHistone DeacetylasesHistones

Identifiers

PMID28819166
PMCPMC5561267
OpenAlexW2742859372

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.