Evidence map›Paper›PMID 29434588›Full record

ArticleFrontiers in immunology2018

GATA3, HDAC6, and BCL6 Regulate FOXP3+ Treg Plasticity and Determine Treg Conversion into Either Novel Antigen-Presenting Cell-Like Treg or Th1-Treg.

Keman Xu, William Y Yang, Gayani Kanchana Nanayakkara, Ying Shao, Fan Yang, Wenhui Hu, Eric T Choi, Hong Wang, Xiaofeng Yang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. 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
3.2field-weighted citation impact, top 8% 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, 74 citations in OpenAlex.

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  15. Tertiary lymphoid structures in colorectal cancer - organization and immune cell interactions.American journal of clinical and experimental immunology · 2024
    Review
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  20. Cigarette Smoke Modulates Inflammation and ImmunityAntioxidants & redox signaling · 2023
    Review
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

9 authors at 1 institution in 1 country.

Keman XuCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
William Y YangCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Gayani Kanchana NanayakkaraCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Ying ShaoCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Fan YangCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Wenhui HuCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Eric T ChoiCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Hong WangCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Xiaofeng YangCenter for Metabolic Disease Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Temple University · US

Funding

CD40 monocyte in chronic kidney diseaseR01DK113775 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2017 to 2021
$3.3M
Hyperhomocysteinemia and HDL MetabolismR01HL117654 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2013 to 2017
$3.0M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
The roles of miR-155 in regulating atherosclerosis and metabolically healthy obesityR01HL138749 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.6M
NADHP Oxidase-mediated MC differentiation & Endothelial Dysfunction in HHcyR01HL110764 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2011 to 2015
$2.5M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
NHLBI NIH HHS R01 HL110764NHLBI NIH HHS R01 HL117654NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL138749NIDDK NIH HHS R01 DK104116NIDDK NIH HHS R01 DK113775
6 · The paper itself

Abstract

We conducted an experimental database analysis to determine the expression of 61 CD4+ Th subset regulators in human and murine tissues, cells, and in T-regulatory cells (Treg) in physiological and pathological conditions. We made the following significant findings: (1) adipose tissues of diabetic patients with insulin resistance upregulated various Th effector subset regulators; (2) in skin biopsy from patients with psoriasis, and in blood cells from patients with lupus, effector Th subset regulators were more upregulated than downregulated; (3) in rosiglitazone induced failing hearts in ApoE-deficient (KO) mice, various Th subset regulators were upregulated rather than downregulated; (4) aortic endothelial cells activated by proatherogenic stimuli secrete several Th subset-promoting cytokines; (5) in Treg from follicular Th (Tfh)-transcription factor (TF) Bcl6 KO mice, various Th subset regulators were upregulated; whereas in Treg from Th2-TF GATA3 KO mice and HDAC6 KO mice, various Th subset regulators were downregulated, suggesting that Bcl6 inhibits, GATA3 and HDAC6 promote, Treg plasticity; and (6) GATA3 KO, and Bcl6 KO Treg upregulated MHC II molecules and T cell co-stimulation receptors, suggesting that GATA3 and BCL6 inhibit Treg from becoming novel APC-Treg. Our data implies that while HDAC6 and Bcl6 are important regulators of Treg plasticity, GATA3 determine the fate of plastic Tregby controlling whether it will convert in to either Th1-Treg or APC-T-reg. Our results have provided novel insights on Treg plasticity into APC-Treg and Th1-Treg, and new therapeutic targets in metabolic diseases, autoimmune diseases, and inflammatory disorders.

Indexed as

AnimalsAntigen-Presenting CellsAortaCell PlasticityEndothelial CellsGATA3 Transcription FactorHistone Deacetylase 6HumansInsulin ResistanceLupus Erythematosus, SystemicLymphocyte ActivationMiceMice, Knockout, ApoEProto-Oncogene Proteins c-bcl-6PsoriasisRosiglitazoneBcl6 protein, mouseGata3 protein, mouseGATA3 Transcription FactorHdac6 protein, mouseHistone Deacetylase 6Proto-Oncogene Proteins c-bcl-6RosiglitazoneAPC-like TregCD4+ FOXP3+ regulatory T cellsCD4+ T helper subset differentiationmetabolic cardiovascular diseasesTh1-like Treg

Identifiers

PMID29434588
PMCPMC5790774
OpenAlexW2787590216

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.