Evidence map›Paper›PMID 14747547›Full record

ArticleJournal of virology2004

A cytomegalovirus inhibitor of gamma interferon signaling controls immunoproteasome induction.

Selina Khan, Albert Zimmermann, Michael Basler, Marcus Groettrup, Hartmut Hengel

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  6. Review
  7. Review
  8. Single-Cell Transcriptome Analysis of CD34Frontiers in microbiology · 2019
    Article
  9. Article
  10. Cytomegalovirus immune evasion of myeloid lineage cells.Medical microbiology and immunology · 2015
    Review
  11. Review
  12. Article
  13. Article
  14. Immune regulation and evasion of Mammalian host cell immunity during viral infection.Indian journal of virology : an official organ of Indian Virological Society · 2013
    Article
  15. Article
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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

5 authors at 3 institutions in 2 countries.

Selina KhanResearch Department, Cantonal Hospital St. Gallen, CH-9007 St. Gallen, Switzerland.
Albert Zimmermann
Michael Basler
Marcus Groettrup
Hartmut Hengel
Robert Koch Institute · DEUniversity of St. Gallen · CHUniversity of Konstanz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both human and mouse cytomegaloviruses (HCMV and MCMV) avoid peptide presentation through the major histocompatibility complex (MHC) class I pathway to CD8(+) T cells. Within the MHC class I pathway, the vast majority of antigenic peptides are generated by the proteasome system, a multicatalytic protease complex consisting of constitutive subunits, three of which can be replaced by enzymatically active gamma interferon (IFN-gamma)-inducible subunits, i.e., LMP2, LMP7, and MECL1, to form the so-called immunoproteasomes. Here, we show that steady-state levels of immunoproteasomes are readily formed in response to MCMV infection in the liver. In contrast, the incorporation of immunoproteasome subunits was prevented in MCMV-infected, as well as HCMV-infected, fibroblasts in vitro. Likewise, the expression of the IFN-gamma-inducible proteasome regulator PA28 alpha beta was also impaired in MCMV-infected cells. Both MCMV and HCMV did not alter the constitutive-subunit composition of proteasomes in infected cells. Quantitative assessment of LMP2, MECL1, and LMP7 transcripts revealed that the inhibition of immunoproteasome formation occurred at a pretranscriptional level. Remarkably, a targeted deletion of the MCMV gene M27, encoding an inhibitor of STAT2 that disrupts IFN-gamma receptor signaling, largely restored transcription and protein expression of immunoproteasome subunits in infected cells. While CMV block peptide transport and MHC class I assembly by posttranslational strategies, immunoproteasome assembly, and thus the repertoire of proteasomal peptides, is controlled by pretranscriptional mechanisms. We hypothesize that the blockade of immunoproteasome formation has considerable consequences for shaping the CD8(+)-T-cell repertoire during the effector phase of the immune response.

Indexed as

Gene Expression RegulationAnimalsCells, CulturedCysteine EndopeptidasesCytomegalovirusCytomegalovirus InfectionsEnzyme InductionFemaleFibroblastsHerpesviridae InfectionsHumansInterferon-gammaMiceMice, Inbred BALB CMuromegalovirusSignal TransductionCysteine EndopeptidasesInterferon-gammaViral Proteins

Identifiers

PMID14747547
PMCPMC369451
OpenAlexW2113029463

What Socratic holds

Textmetadata
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 Socratic graph.