Evidence map›Paper›PMID 23347146›Full record

ReviewImmunology2013

T-cell memory differentiation: insights from transcriptional signatures and epigenetics.

Ben Youngblood, J Scott Hale, Rafi Ahmed

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
  2. The ageing immune system and its battle with viruses.The Journal of general virology · 2026
    Review
  3. Article
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  7. Lower absolute numbers of CD4Renal failure · 2025
    Article
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  9. Review
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  11. Article
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52 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

3 authors at 2 institutions in 1 country.

Ben YoungbloodEmory Vaccine Center, Atlanta, GA, USA.
J Scott Hale
Rafi Ahmed
AID Atlanta · USEmory University · US

Funding

Support Component D/Vaccine Discovery, Concept to ClinicUM1AI100663 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI MCELRATH, MARGARET JULIANA · 2012 to 2018
$131.5M
Targeting the PD-1 signaling pathway to rescue HIV T cell dysfunctionP01AI080192 · NIAID · EMORY UNIVERSITY · PI DUSTIN, MICHAEL LORAN · 2008 to 2012
$12.6M
T CELL MEMORY TO VIRUSESR01AI030048 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AHMED, RAFI · 1990 to 2022
$5.2M
T CELL MEMORY TO VIRUSESR37AI030048 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI · 2001 to 2010
$3.9M
Mechanisms of CD4 T cell help for CD8 T cells during persistent viral infectionF32AI096709 · NIAID · EMORY UNIVERSITY · PI HALE, JEFFREY SCOTT · 2012 to 2013
$110k
NIAID NIH HHS F32 AI096709NIAID NIH HHS P01 AI080192NIAID NIH HHS P01 AI080192-01NIAID NIH HHS R01 AI030048NIAID NIH HHS R37 AI030048NIAID NIH HHS R37 AI30048-17NIAID NIH HHS UM1 AI100663PHS HHS AHMED05GCGH0PHS HHS F32 A1096709-01A1
6 · The paper itself

Abstract

A critical component of vaccine design is to generate and maintain antigen-specific memory lymphocytes of sufficient quantity and quality to give the host life-long protection against re-infection. Therefore, it is important to understand how memory T cells acquire the ability for self-renewal while retaining a potential for heightened recall of effector functions. During acute viral infection or following vaccination, antigen-specific T cells undergo extensive phenotypic and functional changes during differentiation to the effector and memory phases of the immune response. The changes in cell phenotype that accompany memory T-cell differentiation are predominantly mediated through acquired transcriptional regulatory mechanisms, in part achieved through epigenetic modifications of DNA and histones. Here we review our current understanding of epigenetic mechanisms regulating the off-on-off expression of CD8 and CD4 T-cell effector molecules at naive, effector and memory stages of differentiation, respectively, and how covalent modifications to the genome may serve as a mechanism to preserve 'poised' transcriptional states in homeostatically dividing memory cells. We discuss the potential of such mechanisms to control genes that undergo on-off-on patterns of expression including homing and pro-survival genes, and the implications on the development of effector-memory and central-memory T-cell differentiation. Lastly, we review recent studies demonstrating epigenetic modifications as a mechanism for the progressive loss of transcriptional adaptation in antigen-specific T cells that undergo sustained high levels of T-cell receptor signalling.

Indexed as

Cell DifferentiationEpigenomicsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGene Expression RegulationHumansImmunologic MemoryLymphocyte Activation

Identifiers

PMID23347146
PMCPMC3701173
OpenAlexW2044910962

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.