Evidence map›Paper›PMID 25098294›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Activated CD8+ T cells induce expansion of Vβ5+ regulatory T cells via TNFR2 signaling.

Jara J Joedicke, Lara Myers, Aaron B Carmody, Ronald J Messer, Harald Wajant, Karl S Lang, Philipp A Lang, Tak W Mak, Kim J Hasenkrug, Ulf Dittmer

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. TNFRSF1B Is Associated with ANCA in IBD.Inflammatory bowel diseases · 2016
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. The role of TNFR2Life sciences · 2021
    Review
  9. Review
  10. iRhom2: An Emerging Adaptor Regulating Immunity and Disease.International journal of molecular sciences · 2020
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. 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

10 authors at 7 institutions in 3 countries.

Jara J JoedickeInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany;
Lara MyersLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840;
Aaron B CarmodyResearch Technologies Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840;
Ronald J MesserLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840;
Harald WajantDivision of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Würzburg, Würzburg 97080, Germany;
Karl S LangInstitute for Immunology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany;
Philipp A LangDepartment of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Düsseldorf 40225, Germany; Department of Molecular Medicine II, Heinrich-Heine-University Düsseldorf, Düsseldorf 40225, Germany; and.
Tak W MakDepartment of Medical Biophysics and Immunology, The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network, University of Toronto, Toronto, Ontario M5G 2M9, Canada.
Kim J HasenkrugLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; khasenkrug@nih.gov ulf.dittmer@uni-due.de.
Ulf DittmerInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany; khasenkrug@nih.gov ulf.dittmer@uni-due.de.
Essen University Hospital · DENational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · USHeinrich Heine University Düsseldorf · DEUniversitätsklinikum Würzburg · DEUniversity Health Network · CAUniversity of Duisburg-Essen · DE

Funding

Infectious Diseases Research Technologies Core - RMLZICAI001052 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$133.3M
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
Immunology and Pathology of Chronic Murine Leukemia Virus InfectionsZIAAI001100 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2009 to 2015
$3.1M
Intramural NIH HHS ZIA AI001100
6 · The paper itself

Abstract

Vβ5(+) regulatory T cells (Tregs), which are specific for a mouse endogenous retroviral superantigen, become activated and proliferate in response to Friend virus (FV) infection. We previously reported that FV-induced expansion of this Treg subset was dependent on CD8(+) T cells and TNF-α, but independent of IL-2. We now show that the inflammatory milieu associated with FV infection is not necessary for induction of Vβ5(+) Treg expansion. Rather, it is the presence of activated CD8(+) T cells that is critical for their expansion. The data indicate that the mechanism involves signaling between the membrane-bound form of TNF-α on activated CD8(+) T cells and TNFR2 on Tregs. CD8(+) T cells expressing membrane-bound TNF-α but no soluble TNF-α remained competent to induce strong Vβ5(+) Treg expansion in vivo. In addition, Vβ5(+) Tregs expressing only TNFR2 but no TNFR1 were still responsive to expansion. Finally, treatment of naive mice with soluble TNF-α did not induce Vβ5(+) Treg expansion, but treatment with a TNFR2-specific agonist did. These results reveal a new mechanism of intercellular communication between activated CD8(+) T cell effectors and Tregs that results in the activation and expansion of a Treg subset that subsequently suppresses CD8(+) T cell functions.

Indexed as

AnimalsCarrier ProteinsCD8-Positive T-LymphocytesFemaleFriend murine leukemia virusLeukemia, ExperimentalLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-Cell, alpha-betaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRetroviridae InfectionsSignal TransductionT-Lymphocytes, RegulatoryCarrier ProteinsiRhom2 protein, mouseReceptors, Antigen, T-Cell, alpha-betaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIT cell receptor peptide Vbeta5.2Tnfrsf1a protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID25098294
PMCPMC4157120
OpenAlexW1912996546

What OpenQuestion holds

Textmetadata
LicenceTDM
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.