Evidence map›Paper›PMID 25156361›Full record

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

Contribution of TCR signaling strength to CD8+ T cell peripheral tolerance mechanisms.

Trevor R F Smith, Gregory Verdeil, Kristi Marquardt, Linda A Sherman

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. High-affinity oligoclonal TCRs define effective adoptive T cell therapy targeting mutant KRAS-G12D.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Peptide vaccines in cancer-old concept revisited.Current opinion in immunology · 2017
    Review
  13. Article
  14. Regulatory circuits of T cell function in cancer.Nature reviews. Immunology · 2016
    Review
  15. Immune Cells and Inflammation in Diabetic Nephropathy.Journal of diabetes research · 2016
    Review
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Trevor R F SmithDepartment of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.
Gregory VerdeilDepartment of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.
Kristi MarquardtDepartment of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037.
Linda A ShermanDepartment of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037 lsherman@scripps.edu.
Scripps Research Institute · US

Funding

THYMIC AND PERIPHERAL CD8+ T CELL TOLERANCER01DK050824 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI SHERMAN, LINDA A · 1995 to 2014
$5.0M
NIDDK NIH HHS R01 DK050824
6 · The paper itself

Abstract

Peripheral tolerance mechanisms are in place to prevent T cells from mediating aberrant immune responses directed against self and environmental Ags. Mechanisms involved in the induction of peripheral tolerance include T cell-intrinsic pathways, such as anergy or deletion, or exogenous tolerance mediated by regulatory T cells. We have previously shown that the density of peptide-MHC class I recognized by the TCR determines whether CD8(+) T cells undergo anergy or deletion. Specifically, using a TCR-transgenic CD8(+) T cell model, we demonstrated that persistent peripheral exposure to low- or high-dose peptides in the absence of inflammatory signals resulted in clonal deletion or anergy of the T cell, respectively. In this study, by altering the affinity of the peptide-MHC tolerogen for TCR, we have confirmed that this mechanism is dependent on the level of TCR signaling that the CD8(+) T cell receives. Using altered peptide ligands (APLs) displaying high TCR affinities, we show that increasing the TCR signaling favors anergy induction. Conversely, using APLs displaying a decreased TCR affinity tilted our system in the direction of deletional tolerance. We demonstrate how differential peripheral CD8(+) T cell tolerance mechanisms are controlled by both the potency and density of MHC class I-peptide tolerogen.

Indexed as

AnimalsAntigensCD8-Positive T-LymphocytesHistocompatibility Antigens Class IImmune ToleranceMiceMice, Inbred NODMice, KnockoutPeptidesReceptors, Antigen, T-CellAntigensHistocompatibility Antigens Class IPeptidesReceptors, Antigen, T-Cell

Identifiers

PMID25156361
PMCPMC4170000
OpenAlexW2115134592

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.