Evidence map›Paper›PMID 25982319›Full record

ArticleClinical immunology (Orlando, Fla.)2015

Peptide ligand structure and I-Aq binding avidity influence T cell signaling pathway utilization.

Linda K Myers, David L Cullins, Jeoung-Eun Park, Ae-Kyung Yi, David D Brand, Edward F Rosloniec, John M Stuart, Andrew H Kang

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. The role of Syk in peripheral T cells.Clinical immunology (Orlando, Fla.) · 2018
    Article
  2. 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 at 2 institutions in 1 country.

Linda K MyersDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, United States. Electronic address: lmyers@uthsc.edu.
David L CullinsDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States.
Jeoung-Eun ParkDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, United States.
Ae-Kyung YiDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, United States.
David D BrandDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States; Research Service, Veterans Affairs Medical Center, Memphis, TN 38104, United States.
Edward F RosloniecDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States; Research Service, Veterans Affairs Medical Center, Memphis, TN 38104, United States.
John M StuartDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States; Research Service, Veterans Affairs Medical Center, Memphis, TN 38104, United States.
Andrew H KangDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States; Research Service, Veterans Affairs Medical Center, Memphis, TN 38104, United States.
University of Tennessee Health Science Center · USVeterans Health Administration · US

Funding

Immune Suppression of Collagen ArthritisR01AR055661 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MYERS, LINDA K. · 2009 to 2013
$2.1M
20(OH) Vit D3, T Cells, and ArthritisR01AR064825 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANG, ANDREW H · 2014 to 2018
$1.6M
NIAMS NIH HHS AR064825NIAMS NIH HHS AR-55661NIAMS NIH HHS R01 AR055661NIAMS NIH HHS R01 AR064825
6 · The paper itself

Abstract

Factors that drive T cells to signal through differing pathways remain unclear. We have shown that an altered peptide ligand (A9) activates T cells to utilize an alternate signaling pathway which is dependent upon FcRγ and Syk. However, it remains unknown whether the affinity of peptide binding to MHC drives this selection. To answer this question we developed a panel of peptides designed so that amino acids interacting with the p6 and p9 predicted MHC binding pockets were altered. Analogs were tested for binding to I-A(q) using a competitive binding assay and selected analogs were administered to arthritic mice. Using the collagen-induced arthritis (CIA) model, arthritis severity was correlated with T cell cytokine production and molecular T cell signaling responses. We establish that reduced affinity of interaction with the MHC correlates with T cell signaling through the alternative pathway, leading ultimately to secretion of suppressive cytokines and attenuation of arthritis.

Indexed as

AnimalsArthritis, ExperimentalCollagen Type IICytokinesHistocompatibility Antigens Class IILigandsMicePeptide FragmentsPeptidesProtein BindingReceptors, Antigen, T-CellSeverity of Illness IndexSignal TransductionT-LymphocytesCollagen Type IICytokinesHistocompatibility Antigens Class IILigandsPeptide FragmentsPeptidesReceptors, Antigen, T-CellArthritisAutoimmunityT cells

Identifiers

PMID25982319
PMCPMC4959786
OpenAlexW334389425

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.