Evidence map›Paper›PMID 15542669›Full record

ArticleJournal of virology2004

Human cytomegalovirus-specific CD4+-T-cell cytokine response induces fractalkine in endothelial cells.

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

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Fractalkine/CXCells · 2023
    Review
  8. Murine cytomegalovirus promotes renal allograft inflammation via Th1/17 cells and IL-17A.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  9. The Fractalkine Receptor CXFrontiers in immunology · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Cynthia A Bolovan-FrittsDepartment of Pediatrics, University of California at San Diego, 9500 Gilman Dr., 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 GROUPU01AI027563 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SPECTOR, STEPHEN A · 1988 to 2006
$6.4M
PEDIATRIC AIDS--FACTORS IN TRANSMISSION AND PATHOLOGYR01AI039004 · NIAID · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SPECTOR, STEPHEN A · 1995 to 2005
$1.5M
CONCENTRATION-CONTROLLED ANTIRETROVIRAL THERAPYR01AI033835 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI FLETCHER, COURTNEY V. · 1993 to 2005
$1.5M
NIAID NIH HHS AI27563NIAID NIH HHS AI33835NIAID NIH HHS AI36214NIAID NIH HHS AI39004NIAID NIH HHS P30 AI036214NIAID NIH HHS R01 AI033835NIAID NIH HHS R01 AI039004NIAID NIH HHS U01 AI027563
6 · The paper itself

Abstract

Cytomegalovirus (CMV) infection has been linked to inflammation-related disease processes in the human host, including vascular diseases and chronic transplant rejection. The mechanisms through which CMV affects the pathogenesis of these diseases are for the most part unknown. To study the contributing role of the host immune response to CMV in these chronic inflammatory processes, we examined endothelial cell interactions with peripheral blood mononuclear cells (PBMC). Endothelial cultures were monitored for levels of fractalkine induction as a marker for initiating the host inflammatory response. Our results demonstrate that in the presence of CMV antigen PBMC from normal healthy CMV-seropositive donors produce soluble factors that induce fractalkine in endothelial cells. This was not observed in parallel assays with PBMC from seronegative donors. Examination of subset populations within the PBMC further revealed that CMV antigen-stimulated CD4(+) T cells were the source of the factors, gamma interferon and tumor necrosis factor alpha, driving fractalkine induction. Direct contact between CD4(+) cells and the endothelial monolayers is required for this fractalkine induction, where the endothelial cells appear to provide antigen presentation functions. These findings indicate that CMV may represent one member of a class of persistent pathogens where the antigen-specific T-cell response can result in the induction of fractalkine, leading to chronic inflammation and endothelial cell injury.

Indexed as

Antigens, ViralCD4-Positive T-LymphocytesCells, CulturedChemokine CX3CL1Chemokines, CX3CCytokinesCytomegalovirusEndothelial CellsHumansInterferon-gammaLipopolysaccharide ReceptorsMembrane ProteinsTumor Necrosis Factor-alphaAntigens, ViralChemokine CX3CL1Chemokines, CX3CCX3CL1 protein, humanCytokinesInterferon-gammaLipopolysaccharide ReceptorsMembrane ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID15542669
PMCPMC525022
OpenAlexW2107086640

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.