Evidence map›Paper›PMID 21536743›Full record

ArticleThe Journal of experimental medicine2011

Viral persistence redirects CD4 T cell differentiation toward T follicular helper cells.

Laura M Fahey, Elizabeth B Wilson, Heidi Elsaesser, Chris D Fistonich, Dorian B McGavern, David G Brooks

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 322 citations in OpenAlex.

  1. Review
  2. Article
  3. The spontaneous neoantigen-specific CD4Journal for immunotherapy of cancer · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Cell Identity and Spatial Distribution of PD-1/PD-L1 Blockade Responders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. The role of CD4MedComm · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  20. CD4Nature immunology · 2023
    Review

158 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

6 authors at 3 institutions in 1 country.

Laura M FaheyDepartment of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Elizabeth B Wilson
Heidi Elsaesser
Chris D Fistonich
Dorian B McGavern
David G Brooks
University of California, Los Angeles · USBlack AIDS Institute · USNational Institutes of Health · US

Funding

Mechanisms Underlying Clearance of the Persistently Infected CNSZIANS003111 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI MCGAVERN, DORIAN · 2009 to 2025
$33.0M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
Immune Regulation of Viral Persistence and Clearance U01AI082975 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2009 to 2013
$2.0M
NIAID NIH HHS AI 007323NIAID NIH HHS AI 082975NIAID NIH HHS T32 AI007323NIAID NIH HHS U01 AI082975
6 · The paper itself

Abstract

CD4 T cell responses are crucial to prevent and control viral infection; however, virus-specific CD4 T cell activity is considered to be rapidly lost during many persistent viral infections. This is largely caused by the fact that during viral persistence CD4 T cells do not produce the classical Th1 cytokines associated with control of acute viral infections. Considering that CD4 T cell help is critical for both CD8 T cell and B cell functions, it is unclear how CD4 T cells can lose responsiveness but continue to sustain long-term control of persistent viral replication. We now demonstrate that CD4 T cell function is not extinguished as a result of viral persistence. Instead, viral persistence and prolonged T cell receptor stimulation progressively redirects CD4 T cell development away from the Th1 response induced during an acute infection toward T follicular helper cells. Importantly, this sustained CD4 T cell functionality is critical to maintain immunity and ultimately aid in the control of persistent viral infection.

Indexed as

AnimalsB-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationCytokinesLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, KnockoutTh1 CellsCytokines

Identifiers

PMID21536743
PMCPMC3092345
OpenAlexW2147038308

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.