Evidence map›Paper›PMID 24531538›Full record

ArticleCell death and differentiation2014

IRF4 and BATF are critical for CD8⁺ T-cell function following infection with LCMV.

M Grusdat, D R McIlwain, H C Xu, V I Pozdeev, J Knievel, S Q Crome, C Robert-Tissot, R J Dress, A A Pandyra, D E Speiser and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.1field-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

60 citing papers in PubMed, 91 citations in OpenAlex.

  1. Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Transcriptional rewiring in CD8Frontiers in immunology · 2024
    Review
  11. Article
  12. Review
  13. Individual Epitope-Specific CD8Pathogens (Basel, Switzerland) · 2023
    Article
  14. Phosphatidylserine-positive extracellular vesicles boost effector CD8Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  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

25 authors at 7 institutions in 2 countries.

M GrusdatDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
D R McIlwainDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
H C Xu1] Department of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany [2] Institute of Immunology, Medical Faculty, University of Duisburg-Essen, Hufelandstr. 55, Essen 45147, Germany.
V I PozdeevDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
J KnievelDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
S Q CromeDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
C Robert-TissotDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
R J DressInstitute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University of Düsseldorf, Universitätsstr. 1, 40225 Düsseldorf, Germany.
A A PandyraInstitute of Immunology, Medical Faculty, University of Duisburg-Essen, Hufelandstr. 55, Essen 45147, Germany.
D E Speiser1] Department of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1 [2] Clinical Tumor Biology & Immunotherapy Group, Department of Oncology and Ludwig Center for Cancer Research, University of Lausanne HO-05/1552, Av. P.-Decker 4, CH-1011 Lausanne, Switzerland.
E LangDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
S K ManeyDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
A R ElfordDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
S R HamiltonDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
S ScheuInstitute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University of Düsseldorf, Universitätsstr. 1, 40225 Düsseldorf, Germany.
K PfefferInstitute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University of Düsseldorf, Universitätsstr. 1, 40225 Düsseldorf, Germany.
J BodeDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
H-W MittrückerInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M LohoffInstitute for Medical Microbiology and Hospital Hygiene, University of Marburg, Marburg, Germany.
M HuberInstitute for Medical Microbiology and Hospital Hygiene, University of Marburg, Marburg, Germany.
D HäussingerDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
P S OhashiDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
T W MakDepartment of Medical Biophysics and Immunology, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), University of Toronto, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.
K S LangInstitute of Immunology, Medical Faculty, University of Duisburg-Essen, Hufelandstr. 55, Essen 45147, Germany.
P A LangDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEOntario Institute for Cancer Research · CAUniversity Health Network · CAPhilipps University of Marburg · DEUniversity of Duisburg-Essen · DEUniversität Hamburg · DEUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD8(+) T-cell functions are critical for preventing chronic viral infections by eliminating infected cells. For healthy immune responses, beneficial destruction of infected cells must be balanced against immunopathology resulting from collateral damage to tissues. These processes are regulated by factors controlling CD8(+) T-cell function, which are still incompletely understood. Here, we show that the interferon regulatory factor 4 (IRF4) and its cooperating binding partner B-cell-activating transcription factor (BATF) are necessary for sustained CD8(+) T-cell effector function. Although Irf4(-/-) CD8(+) T cells were initially capable of proliferation, IRF4 deficiency resulted in limited CD8(+) T-cell responses after infection with the lymphocytic choriomeningitis virus. Consequently, Irf4(-/-) mice established chronic infections, but were protected from fatal immunopathology. Absence of BATF also resulted in reduced CD8(+) T-cell function, limited immunopathology, and promotion of viral persistence. These data identify the transcription factors IRF4 and BATF as major regulators of antiviral cytotoxic T-cell immunity.

Indexed as

AnimalsApoptosisBasic-Leucine Zipper Transcription FactorsCD8-Positive T-LymphocytesCells, CulturedCytotoxicity, ImmunologicImmunologic MemoryInterferon Regulatory Factor-4Interferon Regulatory FactorsLymphocyte ActivationLymphocytic choriomeningitis virusMice, Inbred C57BLMice, KnockoutBasic-Leucine Zipper Transcription FactorsBatf protein, mouseInterferon Regulatory Factor-4Interferon Regulatory Factors

Identifiers

PMID24531538
PMCPMC4207473
OpenAlexW2074813958

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.