Evidence map›Paper›PMID 24204098›Full record

ArticleMediators of inflammation2013

STAT3 regulates proliferation and survival of CD8+ T cells: enhances effector responses to HSV-1 infection, and inhibits IL-10+ regulatory CD8+ T cells in autoimmune uveitis.

Cheng-Rong Yu, Ivy M Dambuza, Yong-Jun Lee, Gregory M Frank, Charles E Egwuagu

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. IL-21 controls CD8Zoological research · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. CD8Journal of clinical medicine · 2023
    Article
  8. NovelFrontiers in medicine · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. B cell-Derived IL35 Drives STAT3-Dependent CD8Cancer immunology research · 2020
    Article
  13. Article
  14. Activation of the Notch signaling pathway disturbs the CD4Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
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

5 authors at 2 institutions in 1 country.

Cheng-Rong YuMolecular Immunology Section, National Eye Institute, National Institutes of Allergy and Viral Diseases, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD 20892-1857, USA.
Ivy M Dambuza
Yong-Jun Lee
Gregory M Frank
Charles E Egwuagu
National Institutes of Health · USNational Eye Institute · US

Funding

Virus Induction Of Primary CD8 T Cell ResponsesZIAAI000814 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BENNINK, JACK R · 2009 to 2020
$6.8M
Regulation of JAK/STAT pathways in the eyeZIAEY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$5.4M
Antigenic Drift in Influenza A VirusZIAAI001055 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI YEWDELL, JONATHAN W · 2009 to 2015
$3.1M
6 · The paper itself

Abstract

STAT3 regulates CD4+ T cell survival and differentiation. However, its effects on CD8+ T cells are not well understood. Here, we show that in comparison to WT CD8+ T cells, STAT3-deficient CD8+ T cells exhibit a preactivated memory-like phenotype, produce more IL-2, proliferate faster, and are more sensitive to activation-induced cell death (AICD). The enhanced proliferation and sensitivity to AICD correlated with downregulation of class-O forkhead transcription factors (FoxO1, FoxO3A), p21(waf1), p27(KIP1), Bcl-2, OX-40, and upregulation of FasL, Bax, and Bad. We examined whether STAT3-deficient CD8+ T cells can mount effective response during herpes simplex virus (HSV-1) infection and experimental autoimmune uveitis (EAU). Compared to WT mice, HSV-1-infected STAT3-deficient mice (STAT3KO) produced less IFN-γ and virus-specific KLRG-1+ CD8+ T cells. STAT3KO mice are also resistant to EAU and produced less IL-17-producing Tc17 cells. Resistance of STAT3KO to EAU correlated with marked expansion of IL-10-producing regulatory CD8+ T cells (CD8-Treg) implicated in recovery from autoimmune encephalomyelitis. Thus, increases of IL-6-induced STAT3 activation observed during inflammation may inhibit expansion of CD8-Tregs, thereby impeding recovery from uveitis. These results suggest that STAT3 is a potential therapeutic target for upregulating CD8+ T cell-mediated responses to viruses and suggest the successful therapeutic targeting of STAT3 as treatment for uveitis, derived, in part, from promoting CD8-Treg expansion.

Indexed as

AnimalsApoptosisAutoimmune DiseasesCD8-Positive T-LymphocytesCell ProliferationCell SeparationFlow CytometryGene Expression RegulationHerpes SimplexHerpesvirus 1, HumanInflammationInterleukin-10MiceMice, Inbred C57BLMice, KnockoutPhenotypeInterleukin-10Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24204098
PMCPMC3800609
OpenAlexW1562642500

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.