Evidence map›Paper›PMID 21178011›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

A novel role for IFN-stimulated gene factor 3II in IFN-γ signaling and induction of antiviral activity in human cells.

Angel N Morrow, Hana Schmeisser, Takaya Tsuno, Kathryn C Zoon

Open access · greenAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed, 64 citations in OpenAlex.

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  14. The Interferon-Gamma Paradox in Cancer.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Review
  15. Article
  16. Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018
    Review
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Angel N MorrowCytokine Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Hana Schmeisser
Takaya Tsuno
Kathryn C Zoon
National Institute of Allergy and Infectious Diseases · US

Funding

The Antiviral Activities of Human InterferonsZIAAI001039 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ZOON, KATHRYN · 2009 to 2016
$4.3M
Intramural NIH HHS Z99 AI999999NIAID NIH HHS Y99 AI999999
6 · The paper itself

Abstract

Type I (e.g., IFN-α, IFN-β) and type II IFNs (IFN-γ) have antiviral, antiproliferative, and immunomodulatory properties. Both types of IFN signal through the Jak/STAT pathway to elicit antiviral activity, yet IFN-γ is thought to do so only through STAT1 homodimers, whereas type I IFNs activate both STAT1- and STAT2-containing complexes such as IFN-stimulated gene factor 3. In this study, we show that IFN-stimulated gene factor 3 containing unphosphorylated STAT2 (ISGF3(II)) also plays a role in IFN-γ-mediated antiviral activity in humans. Using phosphorylated STAT1 as a marker for IFN signaling, Western blot analysis of IFN-α2a-treated human A549 cells revealed that phospho-STAT1 (Y701) levels peaked at 1 h, decreased by 6 h, and remained at low levels for up to 48 h. Cells treated with IFN-γ showed a biphasic phospho-STAT1 response with an early peak at 1-2 h and a second peak at 15-24 h. Gene expression microarray following IFN-γ treatment for 24 h indicated an induction of antiviral genes that are induced by IFN-stimulated gene factor 3 and associated with a type I IFN response. Induction of these genes by autocrine type I and type III IFN signaling was ruled out using neutralizing Abs to these IFNs in biological assays and by quantitative RT-PCR. Despite the absence of autocrine IFNs, IFN-γ treatment induced formation of ISGF3(II). This novel transcription factor complex binds to IFN-stimulated response element promoter sequences, as shown by chromatin immunoprecipitation analysis of the protein kinase R promoter. STAT2 and IFN regulatory factor 9 knockdown in A549 cells reversed IFN-γ-mediated IFN-stimulated response element induction and antiviral activity, implicating ISGF3(II) formation as a significant component of the cellular response and biological activity of IFN-γ.

Indexed as

AnimalsCell Line, TumorEncephalomyocarditis virusGene Expression ProfilingGene Expression Regulation, ViralHumansInterferon-alphaInterferon-gammaInterferon-Stimulated Gene Factor 3, gamma SubunitMiceOligonucleotide Array Sequence AnalysisPhosphorylationSignal TransductionSTAT1 Transcription FactorIFNA2 protein, humanInterferon-alphaInterferon-gammaInterferon-Stimulated Gene Factor 3, gamma SubunitIRF9 protein, humanSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID21178011
PMCPMC3417313
OpenAlexW2098811581

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.