Evidence map›Paper›PMID 8962123›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Fas-dependent CD4+ cytotoxic T-cell-mediated pathogenesis during virus infection.

A J Zajac, D G Quinn, P L Cohen, J A Frelinger

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Cytotoxic CD4Frontiers in immunology · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Perforin-dependent CD4+ T-cell cytotoxicity contributes to control a murine poxvirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  13. Article
  14. Cytotoxic CD4 T cells in antiviral immunity.Journal of biomedicine & biotechnology · 2011
    Review
  15. Cytolytic CD4(+) T cells in viral immunity.Expert review of vaccines · 2010
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Shaping and reshaping CD8+ T-cell memory.Nature reviews. Immunology · 2008
    Review
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

4 authors at 1 institution in 1 country.

A J ZajacDepartment of Microbiology and Immunology, University of North Carolina, Chapel Hill 27599, USA.
D G Quinn
P L Cohen
J A Frelinger
California Institute of Technology · US

Funding

BASIC IMMUNE MECHANISMST32AI007273 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TISCH, ROLAND M · 1985 to 2020
$5.6M
NIAID NIH HHS AI07273NIAID NIH HHS T32 AI007273PHS HHS A20288
6 · The paper itself

Abstract

beta 2-Microglobulin-deficient (beta 2m-) mice generate a CD4+ major histocompatibility complex class II-restricted cytotoxic T-lymphocyte (CTL) response following infection with lymphocytic choriomeningitis (LCM) virus (LCMV). We have determined the cytotoxic mechanism used by these CD4+ CTLs and have examined the role of this cytotoxic activity in pathogenesis of LCM disease in beta 2m- mice. Lysis of LCMV-infected target cells by CTLs from beta 2m- mice is inhibited by addition of soluble Fas-Ig fusion proteins or by pretreatment of the CTLs with the protein synthesis inhibitor emetine. In addition, LCMV-infected cell lines that are resistant to anti-Fas-induced apoptosis are refractory to lysis by these virus-specific CD4+ CTLs. These data indicate that LCMV-specific CD4+ CTLs from beta 2m- mice use a Fas-dependent lytic mechanism. Intracranial (i.c.) infection of beta 2m- mice with LCMV results in loss of body weight. Fas-deficient beta 2m- Jpr mice develop a similar wasting disease following i.c. infection. This suggests that Fas-dependent cytotoxicity is not required for LCMV-induced weight loss. A potential mediator of this chronic wasting disease is tumor necrosis factor (TNF)-alpha, which is produced by LCMV-specific CD4+ CTLs. In contrast to LCMV-induced weight loss, lethal LCM disease in beta 2m- mice is dependent on Fas-mediated cytotoxicity. Transfer of immune splenocytes from LCMV-infected beta 2m- mice into irradiated infected beta 2m- mice results in death of recipient animals. In contrast, transfer of these splenocytes into irradiated infected beta 2m- Jpr mice does not cause death. Thus a role for CD4+ T-cell-mediated cytotoxicity in virus-induced immunopathology has now been demonstrated.

Indexed as

Cytotoxicity, ImmunologicAdoptive TransferAnimalsbeta 2-MicroglobulinCD4-Positive T-Lymphocytesfas ReceptorHumansLymphocytic ChoriomeningitisMicebeta 2-Microglobulinfas Receptor

Identifiers

PMID8962123
PMCPMC26204
OpenAlexW2161137567

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.