Evidence map›Paper›PMID 28193872›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

NFκB-Pim-1-Eomesodermin axis is critical for maintaining CD8 T-cell memory quality.

Karin M Knudson, Curtis J Pritzl, Vikas Saxena, Amnon Altman, Mark A Daniels, Emma Teixeiro

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. CXCR6 promotes dermal CD8bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Characteristics of CD103Frontiers in cellular and infection microbiology · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. NFκB signaling in T cell memory.Frontiers in immunology · 2023
    Review
  18. Article
  19. Pim1 promotes IFN-β production by interacting with IRF3.Experimental & molecular medicine · 2022
    Article
  20. 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

6 authors at 3 institutions in 1 country.

Karin M KnudsonDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212.
Curtis J PritzlDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212.ORCID 0000-0001-5238-5086
Vikas SaxenaDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212.
Amnon AltmanDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121.
Mark A DanielsDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212.
Emma TeixeiroDepartment of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212; teixeiropernase@missouri.edu.
University of Missouri · USLa Jolla Institute for Immunology · USNational Institutes of Health · US

Funding

T CELLS AND THEIR LYMPHOKINES IN CANCER IMMUNOTHERAPYR01CA035299 · NCI · SCRIPPS RESEARCH INSTITUTE · PI ALTMAN, AMNON · 1985 to 2013
$3.8M
TCR signal transduction in the regulation of T cell memoryR01AI110420 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI TEIXEIRO, EMMA · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA035299NIAID NIH HHS R01 AI110420
6 · The paper itself

Abstract

T-cell memory is critical for long-term immunity. However, the factors involved in maintaining the persistence, function, and phenotype of the memory pool are undefined. Eomesodermin (Eomes) is required for the establishment of the memory pool. Here, we show that in T cells transitioning to memory, the expression of high levels of Eomes is not constitutive but rather requires a continuum of cell-intrinsic NFκB signaling. Failure to maintain NFκB signals after the peak of the response led to impaired Eomes expression and a defect in the maintenance of CD8 T-cell memory. Strikingly, we found that antigen receptor [T-cell receptor (TCR)] signaling regulates this process through expression of the NFκB-dependent kinase proviral integration site for Moloney murine leukemia virus-1 (PIM-1), which in turn regulates NFκB and Eomes. T cells defective in TCR-dependent NFκB signaling were impaired in late expression of Pim-1, Eomes, and CD8 memory. These defects were rescued when TCR-dependent NFκB signaling was restored. We also found that NFκB-Pim-1 signals were required at memory to maintain memory CD8 T-cell longevity, effector function, and Eomes expression. Hence, an NFκB-Pim-1-Eomes axis regulates Eomes levels to maintain memory fitness.

Indexed as

AnimalsCD8-Positive T-LymphocytesImmunologic MemoryMiceMice, Inbred C57BLMoloney murine leukemia virusNF-kappa BReceptors, Antigen, T-CellSignal TransductionT-Box Domain ProteinsNF-kappa BReceptors, Antigen, T-CellT-Box Domain ProteinsCD8 T-cell memoryEomesoderminNFkBPim-1

Identifiers

PMID28193872
PMCPMC5338529
OpenAlexW2588828083

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.