Evidence map›Paper›PMID 23328631›Full record

ArticleCell death and differentiation2013

Reactive oxygen species delay control of lymphocytic choriomeningitis virus.

P A Lang, H C Xu, M Grusdat, D R McIlwain, A A Pandyra, I S Harris, N Shaabani, N Honke, S Kumar Maney, E Lang and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. NK Cells Regulate CD8Frontiers in cellular and infection microbiology · 2020
    Article
  17. A Peroxiredoxin From theFrontiers in cellular and infection microbiology · 2020
    Article
  18. Article
  19. 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

20 authors at 6 institutions in 4 countries.

P A LangInstitute of Experimental Immunology, University Hospital of Zurich, Schmelzbergstrasse 12, Zurich 8091, Switzerland.
H C Xu
M Grusdat
D R McIlwain
A A Pandyra
I S Harris
N Shaabani
N Honke
S Kumar Maney
E Lang
V I Pozdeev
M Recher
B Odermatt
D Brenner
D Häussinger
P S Ohashi
H Hengartner
R M Zinkernagel
T W Mak
K S Lang
Heinrich Heine University Düsseldorf · DEUniversity Hospital of Zurich · CHOntario Institute for Cancer Research · CAUniversity Health Network · CAUniversity of Duisburg-Essen · DEUniversity of Tübingen · DE

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Cluster of differentiation (CD)8(+) T cells are like a double edged sword during chronic viral infections because they not only promote virus elimination but also induce virus-mediated immunopathology. Elevated levels of reactive oxygen species (ROS) have been reported during virus infections. However, the role of ROS in T-cell-mediated immunopathology remains unclear. Here we used the murine lymphocytic choriomeningitis virus to explore the role of ROS during the processes of virus elimination and induction of immunopathology. We found that virus infection led to elevated levels of ROS producing granulocytes and macrophages in virus-infected liver and spleen tissues that were triggered by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Lack of the regulatory subunit p47phox of the NADPH oxidase diminished ROS production in these cells. While CD8(+) T cells exhibited ROS production that was independent of NADPH oxidase expression, survival and T-cell function was elevated in p47phox-deficient (Ncf1(-/-)) mice. In the absence of p47phox, enhanced T-cell immunity promoted virus elimination and blunted corresponding immunopathology. In conclusion, we find that NADPH-mediated production of ROS critically impairs the immune response, impacting elimination of virus and outcome of liver cell damage.

Indexed as

AnimalsButhionine SulfoximineCD8-Positive T-LymphocytesCells, CulturedCell SurvivalDisease Models, AnimalGlutathioneLiverLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutNADPH OxidasesReactive Oxygen SpeciesSpleenButhionine SulfoximineGlutathioneNADPH Oxidasesneutrophil cytosolic factor 1Reactive Oxygen Species

Identifiers

PMID23328631
PMCPMC3595491
OpenAlexW2090530862

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.