Evidence map›Paper›PMID 20693420›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

N-ethyl-N-nitrosourea-induced mutation in ubiquitin-specific peptidase 18 causes hyperactivation of IFN-αß signaling and suppresses STAT4-induced IFN-γ production, resulting in increased susceptibility to Salmonella typhimurium.

Etienne Richer, Caitlin Prendergast, Dong-Er Zhang, Salman T Qureshi, Silvia M Vidal, Danielle Malo

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025
    Review
  3. Article
  4. Article
  5. Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Enterobacteria and host resistance to infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. Multiple functions of USP18.Cell death & disease · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Selective inactivation of USP18 isopeptidase activity in vivo enhances ISG15 conjugation and viral resistance.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  20. Article
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

6 authors at 5 institutions in 3 countries.

Etienne RicherDepartment of Human Genetics, McGill University, Montréal, Québec, Canada.
Caitlin Prendergast
Dong-Er Zhang
Salman T Qureshi
Silvia M Vidal
Danielle Malo
Institute of Human Genetics · PLMcGill Genome Centre · CAMcGill University · CAMcGill University Health Centre · CAUniversity of California, San Diego · US

Funding

Molecular Mechanism of Leukemogenesis Involving AML1-ETOR01CA104509 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2004 to 2025
$6.6M
UBP43 in HematopoiesisR01HL091549 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2008 to 2012
$1.9M
CIHR 87520-1NCI NIH HHS R01 CA104509NHLBI NIH HHS HL091549NHLBI NIH HHS R01 HL091549
6 · The paper itself

Abstract

To deepen our knowledge of the natural host response to pathogens, our team undertook an in vivo screen of mutagenized 129S1 mice with Salmonella Typhimurium. One mutation affecting Salmonella susceptibility was mapped to a region of 1.3 Mb on chromosome 6 that contains 15 protein-coding genes. A missense mutation was identified in the Usp18 (ubiquitin-specific peptidase 18) gene. This mutation results in an increased inflammatory response (IL-6, type 1 IFN) to Salmonella and LPS challenge while paradoxically reducing IFN-gamma production during bacterial infection. Increased STAT1 phosphorylation correlated with impaired STAT4 phosphorylation, resulting in overwhelming IL-6 secretion but reduced IFN-gamma production during infection. The reduced IFN-gamma levels, along with the increased inflammation, rationalize the S. Typhimurium susceptibility in terms of increased bacterial load in target organs and cytokine-induced septic shock and death.

Indexed as

Mutation, MissenseAnimalsEndopeptidasesEthylnitrosoureaFemaleGenetic Predisposition to DiseaseImmunity, InnateInterferon-alphaInterferon-betaInterferon-gammaMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAMice, KnockoutEndopeptidasesEthylnitrosoureaInterferon-alphaInterferon-betaInterferon-gammaMutagensStat4 protein, mouseSTAT4 Transcription FactorUbiquitinUbiquitin ThiolesteraseUsp18 protein, mouse

Identifiers

PMID20693420
PMCPMC3987673
OpenAlexW1936789375

What OpenQuestion holds

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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.