Evidence map›Paper›PMID 23416424›Full record

ArticleMolecular immunology2013

The Bcl6 target gene microRNA-21 promotes Th2 differentiation by a T cell intrinsic pathway.

Deepali V Sawant, Hao Wu, Mark H Kaplan, Alexander L Dent

Abstract read
In one paragraph

Article in Molecular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-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

55 citing papers in PubMed, 95 citations in OpenAlex.

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  16. ncRNAs in Type-2 Immunity.Non-coding RNA · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. MicroRNAs: Potential Biomarkers and Targets of Therapy in Allergic Diseases?Archivum immunologiae et therapiae experimentalis · 2019
    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

4 authors at 2 institutions in 1 country.

Deepali V SawantDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hao Wu
Mark H Kaplan
Alexander L Dent
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

The role of PU.1 in T helper cell heterogeneityR01AI057459 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 2005 to 2025
$8.2M
control of Inflammation by regulatory T cells and BCL6R21AI092297 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI DENT, ALEXANDER L · 2011 to 2012
$424k
Control of autoimmunity by follicular helper T cells and BCL6R21AI090150 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI DENT, ALEXANDER L · 2010 to 2011
$421k
Control of Th2 and Th17 differentiation by BCL6R21AI079349 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI DENT, ALEXANDER L · 2009 to 2010
$385k
Control of airway inflammation and Th2 differentiation by microRNA 21R56AI097607 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI DENT, ALEXANDER L · 2012 to 2012
$193k
NIAID NIH HHS 1R21AI079349-01A1NIAID NIH HHS 1R21AI090150-01NIAID NIH HHS 1R21AI092212-01NIAID NIH HHS R01 AI057459NIAID NIH HHS R21 AI079349NIAID NIH HHS R21 AI090150NIAID NIH HHS R21 AI092297NIAID NIH HHS R56 AI097607
6 · The paper itself

Abstract

The transcriptional repressor Bcl6 is a critical regulator of T helper cell fate, and inhibits Th2-type inflammation. We have found that microRNA-21 (miR-21) is a novel target gene for Bcl6 in Treg cells. Bcl6 represses and Stat3 activates miR-21 transcription through a Stat3 binding element in the promoter, indicating opposing regulation of miR-21 by the two transcription factors via the same DNA site. Ectopic expression of miR-21 promoted Th2 differentiation in non-polarized T cells. The pro-Th2 activity of miR-21 was associated with increased Gata3 expression and decreased expression of the miR-21 target gene Sprouty1. Increased miR-21 promoted Th2 and Treg gene expression in wild-type Tregs. MiR-21 could thus help promote the Th2 bias of Bcl6-deficient conventional T cells and Treg cells. MiR21 expression is increased in Th2-type inflammation, and our results define miR-21 as a critical target of Bcl6, thus providing a new link between Bcl6 and Th2 inflammation. Finally, our results reveal a novel T cell autonomous role for miR-21 in promoting Th2 differentiation.

Indexed as

AnimalsBinding SitesCell DifferentiationDNA-Binding ProteinsInflammationMiceMice, Inbred C57BLMicroRNAsPromoter Regions, GeneticProto-Oncogene Proteins c-bcl-6Repressor ProteinsSTAT3 Transcription FactorTh2 CellsTranscription FactorsBcl6 protein, mouseDNA-Binding ProteinsMicroRNAsMIRN21 microRNA, mouseProto-Oncogene Proteins c-bcl-6Repressor ProteinsStat3 protein, mouseSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID23416424
PMCPMC3602238
OpenAlexW2066491712

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.