Evidence map›Paper›PMID 26824662›Full record

ArticleCell2016

Parsing the Interferon Transcriptional Network and Its Disease Associations.

Sara Mostafavi, Hideyuki Yoshida, Devapregasan Moodley, Hugo LeBoité, Katherine Rothamel, Towfique Raj, Chun Jimmie Ye, Nicolas Chevrier, Shen-Ying Zhang, Ting Feng and 11 more

Abstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 1 pooled it
14.6field-weighted citation impact, top 1% 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

224 citing papers in PubMed, 1 synthesis or guideline pooled it, 342 citations in OpenAlex.

  1. Pooled it
  2. Vitamins DFrontiers in immunology · 2022
    Trial
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164 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

21 authors at 4 institutions in 2 countries.

Sara MostafaviDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA; Department of Statistics and Department Medical Genetics, University of British Columbia, Vancouver, BC V6H 3N1, Canada.
Hideyuki YoshidaDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Devapregasan MoodleyDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Hugo LeBoitéDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Katherine RothamelDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Towfique RajBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Program in Translational NeuroPsychiatric Genomics, Departments of Neurology and Psychiatry, Brigham and Women's Hospital, Boston, MA 02115, USA.
Chun Jimmie YeBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Nicolas ChevrierFAS Center for Systems Biology, Harvard University, Cambridge, MA 02138, USA.
Shen-Ying ZhangSt. Giles Laboratory of Human Genetics of Infectious Diseases, The Rockefeller University, New York, NY 10065, USA.
Ting FengDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Mark LeeBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Jean-Laurent CasanovaSt. Giles Laboratory of Human Genetics of Infectious Diseases, The Rockefeller University, New York, NY 10065, USA.
James D ClarkPfizer Immunosciences, Cambridge, MA 02140, USA.
Martin HegenPfizer Immunosciences, Cambridge, MA 02140, USA.
Jean-Baptiste TelliezPfizer Immunosciences, Cambridge, MA 02140, USA.
Nir HacohenBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Philip L De JagerBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Program in Translational NeuroPsychiatric Genomics, Departments of Neurology and Psychiatry, Brigham and Women's Hospital, Boston, MA 02115, USA.
Aviv RegevBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Diane MathisDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: cbdm@hms.harvard.edu.
Christophe BenoistDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: cbdm@hms.harvard.edu.
Immunological Genome Project Consortium
Harvard University · USBroad Institute · USPfizer (United States) · USRockefeller University · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
ImmGen: Gene Expression and Regulation in Immune CellsR24AI072073 · NIAID · JOSLIN DIABETES CENTER · PI CHRISTOPHE O. BENOIST · 2007 to 2026
$28.5M
Gene Expression and Regulatory Networks in Human LeukocytesRC2GM093080 · NIGMS · HARVARD MEDICAL SCHOOL · PI BENOIST, CHRISTOPHE O., MATHIS, DIANE J · 2009 to 2010
$7.3M
NCI NIH HHS P30 CA014051NIAID NIH HHS R24 AI072073NIAID NIH HHS R24-AI072073NIGMS NIH HHS RC2 GM093080NIGMS NIH HHS RC2-GM093080
6 · The paper itself

Abstract

Type 1 interferon (IFN) is a key mediator of organismal responses to pathogens, eliciting prototypical "interferon signature genes" that encode antiviral and inflammatory mediators. For a global view of IFN signatures and regulatory pathways, we performed gene expression and chromatin analyses of the IFN-induced response across a range of immunocyte lineages. These distinguished ISGs by cell-type specificity, kinetics, and sensitivity to tonic IFN and revealed underlying changes in chromatin configuration. We combined 1,398 human and mouse datasets to computationally infer ISG modules and their regulators, validated by genetic analysis in both species. Some ISGs are controlled by Stat1/2 and Irf9 and the ISRE DNA motif, but others appeared dependent on non-canonical factors. This regulatory framework helped to interpret JAK1 blockade pharmacology, different clusters being affected under tonic or IFN-stimulated conditions, and the IFN signatures previously associated with human diseases, revealing unrecognized subtleties in disease footprints, as affected by human ancestry.

Indexed as

Gene Regulatory NetworksAnimalsCD4-Positive T-LymphocytesDatasets as TopicHumansInterferon Type IJanus KinasesMiceMice, Inbred C57BLReceptor, Interferon alpha-betaInterferon Type IJanus KinasesReceptor, Interferon alpha-beta

Identifiers

PMID26824662
PMCPMC4743492
OpenAlexW2259139274

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.