Evidence map›Paper›PMID 27837109›Full record

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

Characterization of the Syk-Dependent T Cell Signaling Response to an Altered Peptide.

Jeoung-Eun Park, Jeffrey A Rotondo, David L Cullins, David D Brand, Ae-Kyung Yi, John M Stuart, Andrew H Kang, Linda K Myers

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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. The role of Syk in peripheral T cells.Clinical immunology (Orlando, Fla.) · 2018
    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.

Jeoung-Eun ParkDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.
Jeffrey A RotondoDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.ORCID 0000-0001-6123-4722
David L CullinsDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.ORCID 0000-0002-3548-3458
David D BrandDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.ORCID 0000-0002-9260-7963
Ae-Kyung YiDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis TN 38163; and.
John M StuartDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.
Andrew H KangDepartment of Medicine, University of Tennessee Health Science Center, Memphis TN 38163.
Linda K MyersDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis TN 38163 lmyers@uthsc.edu.

Funding

Inhibitory Receptors and Autoimmune ArthritisR01AR069010 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YI, AE-KYUNG · 2016 to 2021
$1.7M
TLR/IL-1R signaling intermediaries and a target-specific therapeutic for arthritiR01AR064723 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YI, AE-KYUNG · 2014 to 2018
$1.6M
20(OH) Vit D3, T Cells, and ArthritisR01AR064825 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANG, ANDREW H · 2014 to 2018
$1.6M
Suppression of Collagen Induced Arthritis with Altered Peptide LigandsR01AR055266 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANG, ANDREW H · 2009 to 2010
$740k
Program Project for Mechanisms and Treatment of ArthritisIP1BX001607 · VA · MEMPHIS VA MEDICAL CENTER · PI BRAND, DAVID D., POSTLETHWAITE, ARNOLD E · 2013 to 2016
–
BLRD VA IP1 BX001607NIAMS NIH HHS R01 AR055266NIAMS NIH HHS R01 AR064723NIAMS NIH HHS R01 AR064825NIAMS NIH HHS R01 AR069010
6 · The paper itself

Abstract

Rheumatoid arthritis is an autoimmune disorder characterized by T cell dysregulation. We have shown that an altered peptide ligand (A9) activates T cells to use an alternate signaling pathway that is dependent on FcRγ and spleen tyrosine kinase, resulting in downregulation of inflammation. In the experiments described in this study, we have attempted to determine the molecular basis of this paradox. Three major Src family kinases found in T cells (Lck, Fyn, and Lyn) were tested for activation following stimulation by A9/I-A

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCalcium SignalingCollagen Type IIHistocompatibility Antigens Class IIHumansInterleukin-10Interleukin-4Lymphocyte ActivationMiceMice, Inbred DBAMice, KnockoutMice, TransgenicPeptide FragmentsReceptors, Antigen, T-Cell, alpha-betaCollagen Type IIHistocompatibility Antigens Class IIInterleukin-10Interleukin-4Peptide FragmentsReceptors, Antigen, T-Cell, alpha-betaReceptors, IgGSyk KinaseSyk protein, mouse

Identifiers

PMID27837109
PMCPMC5714308

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.