Evidence map›Paper›PMID 27521342›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

IL-12 Signals through the TCR To Support CD8 Innate Immune Responses.

Nicholas P Goplen, Vikas Saxena, Karin M Knudson, Adam G Schrum, Diana Gil, Mark A Daniels, Rose Zamoyska, Emma Teixeiro

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. IL17FMolecular medicine (Cambridge, Mass.) · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Expansion of an Unusual Virtual Memory CD8Frontiers in immunology · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

8 authors.

Nicholas P GoplenDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212;ORCID 0000-0003-4614-5996
Vikas SaxenaDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212;ORCID 0000-0003-4816-4875
Karin M KnudsonDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212;
Adam G SchrumDepartment of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905; and.
Diana GilDepartment of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905; and.
Mark A DanielsDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212;
Rose ZamoyskaInstitute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, Ashworth Laboratories, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom.ORCID 0000-0001-9816-2638
Emma TeixeiroDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212; teixeiropernase@missouri.edu.ORCID 0000-0002-3596-5481

Funding

Mechanisms and consequences of CD3 rearrangement during TCR triggeringR01AI097187 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI GIL PAGES, DIANA · 2013 to 2018
$2.0M
TCR signal transduction in the regulation of T cell memoryR01AI110420 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI TEIXEIRO, EMMA · 2015 to 2019
$1.8M
NIAID NIH HHS R01 AI097187NIAID NIH HHS R01 AI110420
6 · The paper itself

Abstract

CD8 T cells must integrate antigenic and inflammatory signals to differentiate into efficient effector and memory T cells able to protect us from infections. The mechanisms by which TCR signaling and proinflammatory cytokine receptor signaling cooperate in these processes are poorly defined. In this study, we show that IL-12 and other proinflammatory cytokines transduce signals through the TCR signalosome in a manner that requires Fyn activity and self-peptide-MHC (self-pMHC) interactions. This mechanism is crucial for CD8 innate T cell functions. Loss of Fyn activity or blockade of self-pMHC interactions severely impaired CD8 T cell IFN-γ and NKG2D expression, proliferation, and cytotoxicity upon cytokine-mediated bystander activation. Most importantly, in the absence of self-pMHC interactions, CD8 memory T cells fail to undergo bystander activation upon an unrelated infection. Thus, CD8 T cell bystander activation, although independent of cognate Ag, still requires self-pMHC and TCR signaling.

Indexed as

Immunity, InnateSignal TransductionAdaptor Proteins, Signal TransducingAnimalsCD8-Positive T-LymphocytesCytokinesCytotoxicity, ImmunologicInterferon-gammaInterleukin-12Lymphocyte ActivationMiceNK Cell Lectin-Like Receptor Subfamily KProtein BindingReceptors, Antigen, T-CellAdaptor Proteins, Signal TransducingCytokinesFyb protein, mouseInterferon-gammaInterleukin-12Klrk1 protein, mouseNK Cell Lectin-Like Receptor Subfamily KReceptors, Antigen, T-Cell

Identifiers

PMID27521342
PMCPMC5010952

What OpenQuestion holds

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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.