Evidence map›Paper›PMID 19178593›Full record

ReviewImmunology2009

Epigenetics and T helper 1 differentiation.

Thomas M Aune, Patrick L Collins, Shaojing Chang

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024
    Review
  5. IFN-γ, should not be ignored in SLE.Frontiers in immunology · 2022
    Review
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  8. 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

3 authors at 2 institutions in 1 country.

Thomas M AuneDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-2068, USA. tom.aune@vanderbilt.edu
Patrick L Collins
Shaojing Chang
Center for Rheumatology · USVanderbilt University · US

Funding

Immunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5M
IFN GAMMA GENE REGULATION IN T CELLS AND NK CELLSR01AI044924 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI AUNE, THOMAS M. · 2000 to 2019
$5.8M
NHLBI NIH HHS T32 HL069765NIAID NIH HHS R01 AI 044924NIAID NIH HHS R01 AI044924
6 · The paper itself

Abstract

Naïve T helper cells differentiate into two subsets, T helper 1 and 2, which either transcribe the Ifng gene and silence the Il4 gene or transcribe the Il4 gene and silence the Ifng gene, respectively. This process is an essential feature of the adaptive immune response to a pathogen and the development of long-lasting immunity. The 'histone code' hypothesis proposes that formation of stable epigenetic histone marks at a gene locus that activate or repress transcription is essential for cell fate determinations, such as T helper 1/T helper 2 cell fate decisions. Activation and silencing of the Ifng gene are achieved through the creation of stable epigenetic histone marks spanning a region of genomic DNA over 20 times greater than the gene itself. Key transcription factors that drive the T helper 1 lineage decision, signal transducer and activator 4 (STAT4) and T-box expressed in T cells (T-bet), play direct roles in the formation of activating histone marks at the Ifng locus. Conversely, STAT6 and GATA binding protein 3, transcription factors essential for the T helper 2 cell lineage decision, establish repressive histone marks at the Ifng locus. Functional studies demonstrate that multiple genomic elements up to 50 kilobases from Ifng play critical roles in its proper transcriptional regulation. Studies of three-dimensional chromatin conformation indicate that these distal regulatory elements may loop towards Ifng to regulate its transcription. We speculate that these complex mechanisms have evolved to tightly control levels of interferon-gamma production, given that too little or too much production would be very deleterious to the host.

Indexed as

Cell DifferentiationChromatinEpigenesis, GeneticHistonesHumansInterferon-gammaTh1 CellsChromatinHistonesInterferon-gamma

Identifiers

PMID19178593
PMCPMC2669810
OpenAlexW2046317156

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.