Evidence map›Paper›PMID 22144897›Full record

ArticlePLoS pathogens2011

A temporal role of type I interferon signaling in CD8+ T cell maturation during acute West Nile virus infection.

Amelia K Pinto, Stephane Daffis, James D Brien, Maria D Gainey, Wayne M Yokoyama, Kathleen C F Sheehan, Kenneth M Murphy, Robert D Schreiber, Michael S Diamond

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
8.5field-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

89 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Human antibodies against West Nile and related orthoflaviviruses.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Mouse models as a tool to study asymptomatic DENV infections.Frontiers in cellular and infection microbiology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

29 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

9 authors at 1 institution in 1 country.

Amelia K PintoDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Stephane Daffis
James D Brien
Maria D Gainey
Wayne M Yokoyama
Kathleen C F Sheehan
Kenneth M Murphy
Robert D Schreiber
Michael S Diamond
Washington University in St. Louis · US

Funding

Virology and Smallpox VaccinationsU54AI057160 · NIAID · WASHINGTON UNIVERSITY · PI RAY, RANJIT · 2003 to 2013
$80.9M
The Burden of Chikungunya and Dengue Infection in KenyaU54AI081680 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI RYMAN, KATHERINE D · 2009 to 2013
$40.4M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
NIAID NIH HHS U19 AI083019NIAID NIH HHS U54 AI057160NIAID NIH HHS U54 AI081680
6 · The paper itself

Abstract

A genetic absence of the common IFN-α/β signaling receptor (IFNAR) in mice is associated with enhanced viral replication and altered adaptive immune responses. However, analysis of IFNAR(-/-) mice is limited for studying the functions of type I IFN at discrete stages of viral infection. To define the temporal functions of type I IFN signaling in the context of infection by West Nile virus (WNV), we treated mice with MAR1-5A3, a neutralizing, non cell-depleting anti-IFNAR antibody. Inhibition of type I IFN signaling at or before day 2 after infection was associated with markedly enhanced viral burden, whereas treatment at day 4 had substantially less effect on WNV dissemination. While antibody treatment prior to infection resulted in massive expansion of virus-specific CD8(+) T cells, blockade of type I IFN signaling starting at day 4 induced dysfunctional CD8(+) T cells with depressed cytokine responses and expression of phenotypic markers suggesting exhaustion. Thus, only the later maturation phase of anti-WNV CD8(+) T cell development requires type I IFN signaling. WNV infection experiments in BATF3(-/-) mice, which lack CD8-α dendritic cells and have impaired priming due to inefficient antigen cross-presentation, revealed a similar effect of blocking IFN signaling on CD8(+) T cell maturation. Collectively, our results suggest that cell non-autonomous type I IFN signaling shapes maturation of antiviral CD8(+) T cell response at a stage distinct from the initial priming event.

Indexed as

Acute DiseaseAnimalsAntibodies, NeutralizingBasic-Leucine Zipper Transcription FactorsCD8 AntigensCD8-Positive T-LymphocytesDendritic CellsInterferon Type IMiceMice, KnockoutReceptor, Interferon alpha-betaRepressor ProteinsSignal TransductionTime FactorsWest Nile FeverWest Nile virusAntibodies, NeutralizingBasic-Leucine Zipper Transcription FactorsCD8 antigen, alpha chainCD8 AntigensInterferon Type IReceptor, Interferon alpha-betaRepressor ProteinsSNFT protein, mouse

Identifiers

PMID22144897
PMCPMC3228803
OpenAlexW2125705042

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.