Evidence map›Paper›PMID 9769336›Full record

ArticleThe Journal of clinical investigation1998

Apoptosis mediated by Fas but not tumor necrosis factor receptor 1 prevents chronic disease in mice infected with murine cytomegalovirus.

M Fleck, E R Kern, T Zhou, J Podlech, W Wintersberger, C K Edwards, J D Mountz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Caspase-8 restricts antiviral CD8 T cell hyperaccumulation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. RIP1 suppresses innate immune necrotic as well as apoptotic cell death during mammalian parturition.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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 3 institutions in 2 countries.

M FleckThe University of Regensburg, Department of Medicine I, 93042 Regensburg, Germany.
E R Kern
T Zhou
J Podlech
W Wintersberger
C K Edwards
J D Mountz
University of Alabama at Birmingham · USAmgen (United States) · USJohannes Gutenberg University Mainz · DE

Funding

GENE THERAPY TO CORRECT ARTHRITIS IN AUTOIMMUNE MICEN01AR062224 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 1996 to 2000
$328k
FAS ANTIGEN AND LIGAND--FUNCTIONAL CHARACTERIZATIONR01AR042547 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 1993 to 1997
–
NIAID NIH HHS R01AI307744NIAMS NIH HHS N01-AR-6-2224NIAMS NIH HHS R01-AR-42547
6 · The paper itself

Abstract

The role of Fas- and TNF-receptor 1 (TNF-R1)-mediated apoptosis in the clearance of virally infected cells and in the regulation of the immune response was analyzed after murine cytomegalovirus (MCMV) infection of C57BL/6 (B6)-+/+ mice, Fas-mutant B6-lpr/lpr mice, TNF-R1 knockout B6-tnfr0/0 mice, and double-deficient B6-tnfr0/0 lpr/lpr mice. There was approximately equivalent clearance of MCMV in B6-+/+, B6-tnfr0/0, and B6-lpr/lpr mice, and by day 28 no infectious virus could be detected in the liver, kidney, lung, or peritoneal exudate. However, delayed virus clearance was observed in B6-tnfr0/0 lpr/lpr mice. An acute inflammatory response occurred in the liver, lung, and kidney of all mice, which was most severe 7 d after MCMV infection, but resolved by day 28 in B6-+/+ and B6-tnfr0/0 mice, but not in B6-lpr/lpr or B6-tnfr0/0 lpr/lpr mice. These results indicate that apoptosis mediated by either Fas or TNF-R1 is sufficient for rapid clearance of the virus. However, apoptosis induced by Fas, but not TNF-R1, is required for the downmodulation of the immune response to the virus and prevention of a chronic inflammatory reaction.

Indexed as

AnimalsAntigens, CDApoptosisChronic DiseaseCytomegalovirus Infectionsfas ReceptorFemaleIn Situ Nick-End LabelingKidneyLiverLungMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalMuromegalovirusAntigens, CDfas ReceptorReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type I

Identifiers

PMID9769336
PMCPMC508991
OpenAlexW2090814843

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.