Evidence map›Paper›PMID 24204252›Full record

ArticlePLoS pathogens2013

Usp18 driven enforced viral replication in dendritic cells contributes to break of immunological tolerance in autoimmune diabetes.

Nadine Honke, Namir Shaabani, Dong-Er Zhang, George Iliakis, Haifeng C Xu, Dieter Häussinger, Mike Recher, Max Löhning, Philipp A Lang, Karl S Lang

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  10. Article
  11. Article
  12. Review
  13. Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020
    Review
  14. Relationship Between Ubiquitin-Specific Peptidase 18 and Hypertension in Polish Adult Male Subjects: A Cross-Sectional Pilot Study.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  15. Article
  16. Vaccines · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 5 institutions in 3 countries.

Nadine HonkeInstitute of Immunology, Faculty of Medicine, University of Duisburg-Essen, Essen, Germany ; Department of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Namir Shaabani
Dong-Er Zhang
George Iliakis
Haifeng C Xu
Dieter Häussinger
Mike Recher
Max Löhning
Philipp A Lang
Karl S Lang
Heinrich Heine University Düsseldorf · DEUniversity of Duisburg-Essen · DEGerman Rheumatism Research Centre · DEUniversity Hospital of Basel · CHUniversity of California, San Diego · US

Funding

UBP43 in HematopoiesisR01HL091549 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2008 to 2012
$1.9M
NHLBI NIH HHS R01 HL091549
6 · The paper itself

Abstract

Infection with viruses carrying cross-reactive antigens is associated with break of immunological tolerance and induction of autoimmune disease. Dendritic cells play an important role in this process. However, it remains unclear why autoimmune-tolerance is broken during virus infection, but usually not during exposure to non-replicating cross-reactive antigens. Here we show that antigen derived from replicating virus but not from non-replicating sources undergoes a multiplication process in dendritic cells in spleen and lymph nodes. This enforced viral replication was dependent on Usp18 and was essential for expansion of autoreactive CD8⁺ T cells. Preventing enforced virus replication by depletion of CD11c⁺ cells, genetically deleting Usp18, or pharmacologically inhibiting of viral replication blunted the expansion of autoreactive CD8⁺ T cells and prevented autoimmune diabetes. In conclusion, Usp18-driven enforced viral replication in dendritic cells can break immunological tolerance and critically influences induction of autoimmunity.

Indexed as

Immune ToleranceAnimalsCD11c AntigenCD8-Positive T-LymphocytesCell LineDendritic CellsDiabetes Mellitus, Type 1Gene DeletionHumansLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, KnockoutUbiquitin ThiolesteraseVirus ReplicationCD11c AntigenUbiquitin ThiolesteraseUsp18 protein, mouse

Identifiers

PMID24204252
PMCPMC3812017
OpenAlexW2021417764

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.