Evidence map›Paper›PMID 19805038›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

The transcription factors T-bet and GATA-3 control alternative pathways of T-cell differentiation through a shared set of target genes.

Richard G Jenner, Michael J Townsend, Ian Jackson, Kaiming Sun, Russell D Bouwman, Richard A Young, Laurie H Glimcher, Graham M Lord

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 3 pooled it
4.9field-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

150 citing papers in PubMed, 3 syntheses or guidelines pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Influence of polyfunctional TbetFrontiers in immunology · 2025
    Trial
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  8. Article
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  15. Review
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  17. Regulatory T cell and endothelial cell crosstalk.Nature reviews. Immunology · 2025
    Review
  18. Article
  19. Natural killer cell granule protein 7 contributes to CD8Research and practice in thrombosis and haemostasis · 2025
    Article
  20. T-betNature communications · 2025
    Article

90 more citing papers are in PubMed but not listed here.

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

8 authors at 6 institutions in 2 countries.

Richard G JennerMRC/UCL Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, London W1T 4JF, United Kingdom. r.jenner@ucl.ac.uk
Michael J Townsend
Ian Jackson
Kaiming Sun
Russell D Bouwman
Richard A Young
Laurie H Glimcher
Graham M Lord
Harvard University · USUniversity College London · GBGuy's and St Thomas' NHS Foundation Trust · GBMassachusetts Institute of Technology · USNational Health Service · GBWhitehead Institute for Biomedical Research · US

Funding

Transcriptional Regulatory Networks in Living CellsR01HG002668 · NHGRI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI YOUNG, RICHARD · 2003 to 2016
$17.9M
Medical Research Council G0600081NHGRI NIH HHS R01 HG002668
6 · The paper itself

Abstract

Upon detection of antigen, CD4(+) T helper (Th) cells can differentiate into a number of effector types that tailor the immune response to different pathogens. Alternative Th1 and Th2 cell fates are specified by the transcription factors T-bet and GATA-3, respectively. Only a handful of target genes are known for these two factors and because of this, the mechanism through which T-bet and GATA-3 induce differentiation toward alternative cell fates is not fully understood. Here, we provide a genomic map of T-bet and GATA-3 binding in primary human T cells and identify their target genes, most of which are previously unknown. In Th1 cells, T-bet associates with genes of diverse function, including those with roles in transcriptional regulation, chemotaxis and adhesion. GATA-3 occupies genes in both Th1 and Th2 cells and, unexpectedly, shares a large proportion of targets with T-bet. Re-complementation of T-bet alters the expression of these genes in a manner that mirrors their differential expression between Th1 and Th2 lineages. These data show that the choice between Th1 and Th2 lineage commitment is the result of the opposing action of T-bet and GATA-3 at a shared set of target genes and may provide a general paradigm for the interaction of lineage-specifying transcription factors.

Indexed as

Cell DifferentiationChromatin ImmunoprecipitationGATA3 Transcription FactorGenes, MHC Class IIHumansIn Vitro TechniquesOligonucleotide Array Sequence AnalysisT-bet Transcription FactorT-Box Domain ProteinsTh1 CellsTh2 CellsTranscriptional ActivationGATA3 protein, humanGATA3 Transcription FactorT-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID19805038
PMCPMC2764903
OpenAlexW1965759657

What OpenQuestion holds

Textmetadata
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.