Evidence map›Paper›PMID 30266866›Full record

ArticleScience immunology2018

The probacterial effect of type I interferon signaling requires its own negative regulator USP18.

Namir Shaabani, Nadine Honke, Nhan Nguyen, Zhe Huang, Kei-Ichiro Arimoto, Daniel Lazar, Taylor K Loe, Karl S Lang, Marco Prinz, Klaus-Peter Knobeloch and 2 more

Open access · greenAbstract read
In one paragraph

Article in Science immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020
    Review
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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

12 authors at 5 institutions in 2 countries.

Namir ShaabaniDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA. shaabani@scripps.edu teijaro@scripps.edu.ORCID 0000-0003-3548-5899
Nadine HonkeInstitute of Immunology, Faculty of Medicine, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0002-2220-6806
Nhan NguyenDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Zhe HuangDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.ORCID 0000-0002-1312-5457
Kei-Ichiro ArimotoMoores UCSD Cancer Center, University of California San Diego, La Jolla, CA 92093, USA.
Daniel LazarDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.ORCID 0000-0002-1130-4590
Taylor K LoeDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Karl S LangInstitute of Immunology, Faculty of Medicine, University of Duisburg-Essen, Essen, Germany.
Marco PrinzInstitute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany.
Klaus-Peter KnobelochInstitute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany.ORCID 0000-0003-1587-1944
Dong-Er ZhangMoores UCSD Cancer Center, University of California San Diego, La Jolla, CA 92093, USA.ORCID 0000-0003-2541-6443
John R TeijaroDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA. shaabani@scripps.edu teijaro@scripps.edu.ORCID 0000-0001-8280-8887
Scripps Research Institute · USUniversity of California San Diego · USUniversity of Freiburg · DEDüsseldorf University Hospital · DEUniversity of Duisburg-Essen · DE

Funding

ISG15 and Protein ISGylation in CancerR01CA177305 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2013 to 2023
$3.7M
Novel Strategies for Controlling Persistent Viral InfectionR01AI123210 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI TEIJARO, JOHN ROSS · 2016 to 2019
$1.9M
NCI NIH HHS R01 CA177305NIAID NIH HHS R01 AI123210
6 · The paper itself

Abstract

Type I interferon (IFN-I) signaling paradoxically impairs host immune responses during many primary and secondary bacterial infections. Lack of IFN-I receptor reduces bacterial replication and/or bacterial persistence during infection with several bacteria. However, the mechanisms that mediate the adverse IFN-I effect are incompletely understood. Here, we show that

Indexed as

AnimalsFemaleInterferon Type IListeria monocytogenesListeriosisMaleMice, TransgenicReceptor, Interferon alpha-betaSignal TransductionStaphylococcal InfectionsStaphylococcus aureusTumor Necrosis Factor-alphaUbiquitin ThiolesteraseIfnar1 protein, mouseInterferon Type IReceptor, Interferon alpha-betaTumor Necrosis Factor-alphaUbiquitin ThiolesteraseUsp18 protein, mouse

Identifiers

PMID30266866
PMCPMC6408137
OpenAlexW2893590114

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.