Evidence map›Paper›PMID 16652169›Full record

ArticlePLoS pathogens2006

Foxp3 represses retroviral transcription by targeting both NF-kappaB and CREB pathways.

Christian Grant, Unsong Oh, Kazunori Fugo, Norihiro Takenouchi, Caitlin Griffith, Karen Yao, Timothy E Newhook, Lee Ratner, Steven Jacobson

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.9field-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

41 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
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  5. Review
  6. Article
  7. Regulatory T cells: the ultimate HIV reservoir?Journal of virus eradication · 2018
    Article
  8. CD4AIDS research and human retroviruses · 2018
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
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  16. 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

9 authors at 3 institutions in 1 country.

Christian GrantViral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.
Unsong Oh
Kazunori Fugo
Norihiro Takenouchi
Caitlin Griffith
Karen Yao
Timothy E Newhook
Lee Ratner
Steven Jacobson
National Institutes of Health · USNational Institute of Neurological Disorders and Stroke · USWashington University in St. Louis · US

Funding

Involvement Of Human Viruses Associated With Chronic Neurologic DiseaseZIANS002817 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI JACOBSON, STEVEN · 2009 to 2025
$26.5M
Retrovirus Associated With Chronic Neurologic DiseaseZ01NS002817 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI JACOBSON, STEVEN · 1990 to 2008
$4.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Forkhead box (Fox)/winged-helix transcription factors regulate multiple aspects of immune responsiveness and Foxp3 is recognized as an essential functional marker of regulatory T cells. Herein we describe downstream signaling pathways targeted by Foxp3 that may negatively impact retroviral pathogenesis. Overexpression of Foxp3 in HEK 293T and purified CD4+ T cells resulted in a dose-dependent and time-dependent decrease in basal levels of nuclear factor-kappaB (NF-kappaB) activation. Deletion of the carboxyl-terminal forkhead (FKH) domain, critical for nuclear localization and DNA-binding activity, abrogated the ability of Foxp3 to suppress NF-kappaB activity in HEK 293T cells, but not in Jurkat or primary human CD4+ T cells. We further demonstrate that Foxp3 suppressed the transcription of two human retroviral promoters (HIV-1 and human T cell lymphotropic virus type I [HTLV-I]) utilizing NF-kappaB-dependent and NF-kappaB-independent mechanisms. Examination of the latter identified the cAMP-responsive element binding protein (CREB) pathway as a target of Foxp3. Finally, comparison of the percent Foxp3+CD4+CD25+ T cells to the HTLV-I proviral load in HTLV-I-infected asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis suggested that high Foxp3 expression is associated with low proviral load and absence of disease. These results suggest an expanded role for Foxp3 in regulating NF-kappaB- and CREB-dependent cellular and viral gene expression.

Indexed as

Transcription, GeneticCD4-Positive T-LymphocytesCREB-Binding ProteinForkhead Transcription FactorsGene Expression Regulation, ViralGene TargetingHumansJurkat CellsKidneyLeukocytes, MononuclearNF-kappa BRetroviridaeReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCREB-Binding ProteinCREBBP protein, humanForkhead Transcription FactorsFOXP3 protein, humanNF-kappa BRNA, Messenger

Identifiers

PMID16652169
PMCPMC1447668
OpenAlexW2050938549

What OpenQuestion holds

Textmetadata
LicenceCC0
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.