Evidence map›Paper›PMID 17519388›Full record

ArticleBlood2007

High T-cell response to human cytomegalovirus induces chemokine-mediated endothelial cell damage.

Cynthia A Bolovan-Fritts, Rodney N Trout, Stephen A Spector

Open access · greenAbstract read
In one paragraph

Article in Blood, 2007. 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
1.0field-weighted citation impact, top 23% 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, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Fractalkine/CXCells · 2023
    Review
  8. Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022
    Review
  9. The Fractalkine Receptor CXFrontiers in immunology · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cytomegalovirus and HIV: A Dangerous Pas de Deux.The Journal of infectious diseases · 2016
    Review
  17. Review
  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

3 authors at 2 institutions in 1 country.

Cynthia A Bolovan-FrittsDepartment of Pediatrics, Division of Infectious Diseases, University of California San Diego, La Jolla, CA 92093-0672, USA.
Rodney N Trout
Stephen A Spector
Office of Infectious Diseases · USUniversity of California, San Diego · US

Funding

VirologyP30AI036214 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Maile Ann Young Karris · 1994 to 2026
$78.4M
PEDIATRIC AIDS CLINICAL TRIALS GROUP--COORDINATE/OPERATEU01AI041089 · NIAID · SOCIAL AND SCIENTIFIC SYSTEMS, INC. · PI SPECTOR, STEPHEN A · 1997 to 2005
$71.9M
NIAID NIH HHS AI-36 214NIAID NIH HHS AI-41 089
6 · The paper itself

Abstract

Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial damage, including vascular disease and chronic transplant rejection. We previously reported that the host CD4(+) T-cell response to CMV antigen presented by endothelial cells can produce interferon-gamma and tumor necrosis factor-alpha at levels sufficient to drive induction of fractalkine, a key marker of inflammation, in endothelial cells. In this work, we report that donors with high frequencies of antigen-specific T cells to CMV (high responders) induce higher levels of activation-associated chemokines such as fractalkine, RANTES (regulated on activation, normal T cell expressed and secreted), and macrophage inflammatory protein-1beta, together with cell-adhesion markers in endothelial cells compared with donors with low levels of CMV-specific T cells (low responders). High-responder cultures had higher levels of leukocyte recruitment and adherence to the endothelial monolayers associated with progressive damage and loss of the endothelial cells. These processes that led to endothelial destruction only required viral antigen and did not require infectious virus. Our findings further support that CMV may represent one member of a class of persistent pathogens in which a high antigen-specific T-cell response defines an important risk factor for development of chronic inflammation and endothelial cell injury.

Indexed as

Antigens, ViralAortaCD4-Positive T-LymphocytesCell AdhesionCell MovementCells, CulturedChemokine CCL4Chemokine CCL5CytomegalovirusCytomegalovirus InfectionsEndothelium, VascularEnzyme-Linked Immunosorbent AssayFibroblastsFlow CytometryHumansIntercellular Adhesion Molecule-1Antigens, ViralChemokine CCL4Chemokine CCL5Intercellular Adhesion Molecule-1Interferon-gammaMacrophage Inflammatory ProteinsVascular Cell Adhesion Molecule-1

Identifiers

PMID17519388
PMCPMC1976357
OpenAlexW2046858006

What OpenQuestion 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 OpenQuestion graph.