Evidence map›Paper›PMID 21255624›Full record

ArticleVirus research2011

Regulation of STAT signaling in mouse bone marrow derived dendritic cells by respiratory syncytial virus.

Zhijun Jie, Darrell L Dinwiddie, Albert P Senft, Kevin S Harrod

Abstract read
In one paragraph

Article in Virus research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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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

4 authors at 1 institution in 2 countries.

Zhijun JieInfectious Diseases Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. jiezjlxh@gmail.com
Darrell L Dinwiddie
Albert P Senft
Kevin S Harrod
Lovelace Respiratory Research Institute · US

Funding

CCSP IN INNATE DEFENSE AGAINST LUNG VIRAL INFECTIONR01HL066964 · NHLBI · LOVELACE BIOMEDICAL &ENVIRONMENTAL RES · PI HARROD, KEVIN S · 2000 to 2003
$1.4M
Molecular Physiology of Extracellular Fluid BalanceK22HL066994 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MASILAMANI, SHYAMA · 2004 to 2005
$370k
NHLBI NIH HHS HL-66994NHLBI NIH HHS K22 HL066994NHLBI NIH HHS R01 HL066964
6 · The paper itself

Abstract

BACKGROUND/

aimsDendritic cells (DCs) act as a portal for virus invasion as well as potent antigen-presenting cells (APCs) involved in the antiviral host response. Interferons (IFNs) are produced in response to bacterial and viral infection and activate innate immune responses to efficiently counteract and remove pathogenic invaders. Respiratory syncytial virus (RSV) could inhibit IFN-mediated signaling pathway in epithelial cells; however, the effects of RSV on IFN signaling in the dendritic cells (DCs) are still unknown.

methodsMouse bone marrow derived DCs (BMDCs) were mock or infected with RSV at different multiplicity of infection (MOI) for 24h, and then treated with different cytokines such as interferon-β (IFN-β), IFN-γ or interleukin-10 (IL-10). The mRNA expression of RSV nonstructural protein-1 (NS-1) and NS-2 was detected by RT-PCR. The expression of Janus family kinase-signal transducer and activator of transcription (JAK/STAT) signaling proteins was assessed by immunoblotting assays. The nuclear localization of specific signaling proteins was determined by immunofluorescence assay.

resultsIncreasing amounts of NS-1 or NS-2 mRNA expression in BMDCs were observed with infected RSV at increasing MOI, suggesting BMDCs were permissive for viral gene expression. Further examination of the IFN-β signaling cascade showed RSV infection increased the total cellular levels of STAT1 and STAT2 in BMDCs, but impaired the IFN-β-dependent phosphorylation and nuclear localization of STAT1 and STAT2. The inhibitory effects of RSV on STAT1 and STAT2 phosphorylation and translocation were abolished by UV inactivation. In contrast, RSV did not inhibit the IFN-γ-stimulated STAT1 phosphorylation and nuclear localization. IL-10-stimulated STAT3 phosphorylation was also unaffected by RSV.

conclusionsAs well as RSV inhibiting STAT protein levels through degradation mechanisms in epithelial cells, these findings demonstrate that RSV also can specifically inhibit the type I interferon response in BMDCs through regulation of STAT1 and STAT2 phosphorylation and nuclear translocation.

Indexed as

Signal TransductionAnimalsBone Marrow CellsCell NucleusCells, CulturedDendritic CellsInterferonsInterleukin-10MiceMice, Inbred BALB CRespiratory Syncytial VirusesSTAT Transcription FactorsVirus ReplicationInterferonsInterleukin-10STAT Transcription Factors

Identifiers

PMID21255624
PMCPMC3726278
OpenAlexW2078475189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.