Evidence map›Paper›PMID 10933693›Full record

ArticleJournal of virology2000

Macrophages escape inhibition of major histocompatibility complex class I-dependent antigen presentation by cytomegalovirus.

H Hengel, U Reusch, G Geginat, R Holtappels, T Ruppert, E Hellebrand, U H Koszinowski

Abstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cytomegalovirus inhibition of extrinsic apoptosis determines fitness and resistance to cytotoxic CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. Article
  6. Review
  7. Article
  8. Cytomegalovirus immune evasion of myeloid lineage cells.Medical microbiology and immunology · 2015
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. MHC class I immune evasion in MCMV infection.Medical microbiology and immunology · 2008
    Review
  14. Article
  15. Article
  16. Article
  17. 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

7 authors at 2 institutions in 1 country.

H HengelLehrstuhl Virologie, Max von Pettenkofer-Institut, Ludwig-Maximilians-Universität, 80336 Munich, Germany. hengelh@rki.de
U Reusch
G Geginat
R Holtappels
T Ruppert
E Hellebrand
U H Koszinowski
Ludwig-Maximilians-Universität München · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mouse cytomegalovirus (MCMV) m152- and m06-encoded glycoproteins gp40 and gp48, respectively, independently downregulate major histocompatibility complex (MHC) class I surface expression during the course of productive MCMV infection in fibroblasts. As a result, presentation of an immediate-early protein pp89-derived nonapeptide to H-2L(d)-restricted CD8(+) cytotoxic T cells is completely prevented in fibroblasts. Here we demonstrate that MCMV-infected primary bone marrow macrophages and the macrophage cell line J774 constitutively present pp89 peptides during permissive MCMV infection to cytotoxic T lymphocytes (CTL). In contrast to fibroblasts, expression of the m152 and m06 genes in macrophages does not affect surface expression of MHC class I. Assessment of pp89 synthesis and quantification of extracted peptide revealed a significantly higher efficiency of macrophages than of fibroblasts to process pp89 into finally trimmed peptide. The yield of pp89 peptide determined in MCMV-infected tissues of bone marrow chimeras confirmed that bone marrow-derived cells represent a prime source of pp89 processing in parenchymal organs. The finding that macrophages resist the viral control of MHC I-dependent antigen presentation reconciles the paradox of efficient induction of CMV-specific CD8(+) CTL in vivo despite extensive potential of CMVs to subvert MHC class I.

Indexed as

Antigen PresentationAnimalsBone Marrow CellsCD8-Positive T-LymphocytesCell LineCytomegalovirusHistocompatibility Antigens Class IImmediate-Early ProteinsMacrophagesMembrane GlycoproteinsMiceMice, Inbred BALB CViral Envelope ProteinsViral Proteinscytomegalovirus immediate early phosphoprotein pp89Histocompatibility Antigens Class IImmediate-Early Proteinsm152 protein, cytomegalovirusMembrane GlycoproteinsUL4 protein, Human cytomegalovirusViral Envelope ProteinsViral Proteins

Identifiers

PMID10933693
PMCPMC112316
OpenAlexW2150467115

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.