Evidence map›Paper›PMID 31471108›Full record

ArticleImmunity2019

Differential Activation of the Transcription Factor IRF1 Underlies the Distinct Immune Responses Elicited by Type I and Type III Interferons.

Adriana Forero, Snehal Ozarkar, Hongchuan Li, Chia Heng Lee, Emily A Hemann, Marija S Nadjsombati, Matthew R Hendricks, Lomon So, Richard Green, Chandra N Roy and 5 more

Open access · greenAbstract read
In one paragraph

Article in Immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed
11.7field-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

184 citing papers in PubMed, 264 citations in OpenAlex.

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124 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Adriana ForeroDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Snehal OzarkarDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Hongchuan LiBasic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Chia Heng LeeDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Emily A HemannDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Marija S NadjsombatiDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Matthew R HendricksDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Lomon SoDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Richard GreenDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA 98109, USA.
Chandra N RoyUniversity of Pittsburgh Cancer Institute, Pittsburgh, PA 15232, USA.
Saumendra N SarkarUniversity of Pittsburgh Cancer Institute, Pittsburgh, PA 15232, USA.
Jakob von MoltkeDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA.
Stephen K AndersonBasic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA; Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA.
Michael GaleDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA 98109, USA.
Ram SavanDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98109, USA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA 98109, USA. Electronic address: savanram@uw.edu.
University of Washington · USUPMC Hillman Cancer Center · USAlpine Immune Sciences (United States) · USFrederick National Laboratory for Cancer Research · USNational Cancer Institute · US

Funding

Washington National Primate Research CenterP51OD010425 · OD · UNIVERSITY OF WASHINGTON · PI Mari Ostendorf · 2012 to 2026
$201.8M
Unlocking Zika Virus Immune Control and Pathogenesis with the Collaborative CrossU19AI100625 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MCWEENEY, SHANNON K. · 2012 to 2021
$36.6M
EXPERIMENTAL PATHOLOGY OF CARDIOVASCULAR DISEASET32HL007312 · NHLBI · UNIVERSITY OF WASHINGTON · PI MAJESKY, MARK W., SCHWARTZ, STEPHEN MARK · 1985 to 2019
$11.8M
Diseases of Public Health Importance Training GrantT32AI007509 · NIAID · UNIVERSITY OF WASHINGTON · PI LUND, JENNIFER M · 1997 to 2024
$6.3M
Innate Immune Control of West Nile VirusR01AI104002 · NIAID · UNIVERSITY OF WASHINGTON · PI DIAMOND, MICHAEL S, GALE, MICHAEL · 2013 to 2017
$3.7M
Mechanisms of hepatic innate immune activation by HCVR01AI127463 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL, ROSEN, HUGO RAMON · 2017 to 2021
$2.8M
Sensing of helminths by tuft cellsDP2AI136596 · NIAID · UNIVERSITY OF WASHINGTON · PI VON MOLTKE, JAKOB H. · 2017 to 2017
$2.6M
The Host Response to Hepatitis C VirusR01AI118916 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2016 to 2020
$2.5M
Novel regulatory mechanisms control IFNL3 expression during HCV infectionR01AI108765 · NIAID · UNIVERSITY OF WASHINGTON · PI SAVAN, RAM · 2014 to 2018
$2.3M
Differential modulation of RIG-I and cGAS signaling by OASL and its role in antiviral response.R01AI118896 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SARKAR, SAUMENDRA N · 2015 to 2019
$2.1M
Creation of Immuno-Oncolytic Viruses for Cancer TherapyR01CA178766 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SARKAR, SAUMENDRA N · 2014 to 2018
$1.6M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS R01 CA178766NHLBI NIH HHS T32 HL007312NIAID NIH HHS DP2 AI136596NIAID NIH HHS R01 AI104002NIAID NIH HHS R01 AI108765NIAID NIH HHS R01 AI118896NIAID NIH HHS R01 AI118916NIAID NIH HHS R01 AI127463NIAID NIH HHS T32 AI007509NIAID NIH HHS U19 AI100625NIH HHS P51 OD010425
6 · The paper itself

Abstract

Type I and III interferons (IFNs) activate similar downstream signaling cascades, but unlike type I IFNs, type III IFNs (IFNλ) do not elicit strong inflammatory responses in vivo. Here, we examined the molecular mechanisms underlying this disparity. Type I and III IFNs displayed kinetic differences in expression of IFN-stimulated genes and proinflammatory responses, with type I IFNs preferentially stimulating expression of the transcription factor IRF1. Type III IFNs failed to induce IRF1 expression because of low IFNλ receptor abundance and insufficient STAT1 activation on epithelial cells and thus did not activate the IRF1 proinflammatory gene program. Rather, IFNλ stimulation preferentially induced factors implicated in tissue repair. Our findings suggest that IFN receptor compartmentalization and abundance confer a spatiotemporal division of labor where type III IFNs control viral spread at the site of the infection while restricting tissue damage; the transient induction of inflammatory responses by type I IFNs recruits immune effectors to promote protective immunity.

Indexed as

AnimalsCell LineEpithelial CellsHumansInflammationInterferon LambdaInterferon Regulatory Factor-1InterferonsInterferon Type IMaleMiceMice, Inbred C57BLSTAT1 Transcription FactorInterferon LambdaInterferon Regulatory Factor-1InterferonsInterferon Type IIRF1 protein, humanSTAT1 Transcription Factorchemokinesepithelial cellsinflammationinterferon lambdainterferon regulatory factor 1interferons

Identifiers

PMID31471108
PMCPMC7447158
OpenAlexW2970141704

What OpenQuestion holds

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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.