Evidence map›Paper›PMID 28798348›Full record

ArticleScientific reports2017

Fas Ligand-mediated cytotoxicity of CD4+ T cells during chronic retrovirus infection.

Anna Malyshkina, Elisabeth Littwitz-Salomon, Kathrin Sutter, Gennadiy Zelinskyy, Sonja Windmann, Simone Schimmer, Annette Paschen, Hendrik Streeck, Kim J Hasenkrug, Ulf Dittmer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
1.5field-weighted citation impact, top 19% 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, 32 citations in OpenAlex.

  1. Article
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  6. FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025
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  12. Cytotoxic CD4Frontiers in immunology · 2023
    Review
  13. Article
  14. Host immune response against DENV and ZIKV infections.Frontiers in cellular and infection microbiology · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. T Cell Reprogramming Against Cancer.Methods in molecular biology (Clifton, N.J.) · 2020
    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

10 authors at 3 institutions in 2 countries.

Anna MalyshkinaInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany. Anna.Malyshkina@uk-essen.de.ORCID 0000-0001-5199-5472
Elisabeth Littwitz-SalomonInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Kathrin SutterInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Gennadiy ZelinskyyInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Sonja WindmannInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Simone SchimmerInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Annette PaschenDepartment of Dermatology, Venereology, and Allergology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Hendrik StreeckInstitute for HIV Research, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Kim J HasenkrugLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA.
Ulf DittmerInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DEEssen University Hospital · DENational Institutes of Health · US

Funding

Immunology And Pathology Of Acute Murine Leukemia Virus InfectionsZIAAI000753 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2009 to 2022
$8.1M
6 · The paper itself

Abstract

CD4+ helper T cells and cytotoxic CD8+ T cells are key players for adaptive immune responses against acute infections with retroviruses. Similar to textbook knowledge the most important function of CD4+ T cells during an acute retrovirus infection seems to be their helper function for other immune cells. Whereas there was no direct anti-viral activity of CD4+ T cells during acute Friend Virus (FV) infection, they were absolutely required for the control of chronic infection. During chronic FV infection a population of activated FV-specific CD4+ T cells did not express cytotoxic molecules, but Fas Ligand that can induce Fas-induced apoptosis in target cells. Using an MHC II-restricted in vivo CTL assay we demonstrated that FV-specific CD4+ T cells indeed mediated cytotoxic effects against FV epitope peptide loaded targets. CD4 + CTL killing was also detected in FV-infected granzyme B knockout mice confirming that the exocytosis pathway was not involved. However, killing could be blocked by antibodies against FasL, which identified the Fas/FasL pathway as critical cytotoxic mechanism during chronic FV infection. Interestingly, targeting the co-stimulatory receptor CD137 with an agonistic antibody enhanced CD4+ T cell cytotoxicity. This immunotherapy may be an interesting new approach for the treatment of chronic viral infections.

Indexed as

Cytotoxicity, ImmunologicAnimalsApoptosisCD4-Positive T-LymphocytesCells, CulturedFas Ligand ProteinFemaleFriend murine leukemia virusLeukemia, ExperimentalMiceMice, Inbred C57BLRetroviridae InfectionsTumor Virus InfectionsFas Ligand Protein

Identifiers

PMID28798348
PMCPMC5552859
OpenAlexW2743531044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.