Evidence map›Paper›PMID 28887430›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

The Role of Leukocyte-Associated Ig-like Receptor-1 in Suppressing Collagen-Induced Arthritis.

Seunghyun Kim, Ellis R Easterling, Lauren C Price, Savannah L Smith, John E Coligan, Jeoung-Eun Park, David D Brand, Edward F Rosloniec, John M Stuart, Andrew H Kang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  16. Roles of PLODs in Collagen Synthesis and Cancer Progression.Frontiers in cell and developmental biology · 2018
    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

11 authors at 2 institutions in 1 country.

Seunghyun KimDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.
Ellis R EasterlingDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.
Lauren C PriceDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.
Savannah L SmithDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.
John E ColiganReceptor Cell Biology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, Rockville, MD 20852.
Jeoung-Eun ParkDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0002-4080-4447
David D BrandDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0002-9260-7963
Edward F RosloniecDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163.
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 MyersDivision of Rheumatology, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163 lmyers@uthsc.edu.
University of Tennessee Health Science Center · USNational Institute of Allergy and Infectious Diseases · US

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
NIAMS NIH HHS R01 AR064723NIAMS NIH HHS R01 AR064825NIAMS NIH HHS R01 AR069010
6 · The paper itself

Abstract

Several observations implicate a critical role for T cell dysregulation as a central problem in rheumatoid arthritis. We investigated a mechanism for suppressing T cell activation by stimulating a natural inhibitory receptor called leukocyte-associated Ig-like receptor-1 (LAIR-1). The collagen-induced arthritis (CIA) model and DR-1 transgenic mice were used to study the importance of LAIR-1 in autoimmune arthritis. Splenocytes from wild-type or LAIR-1

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCD4-Positive T-LymphocytesCells, CulturedCollagen Type IIDisease Models, AnimalHLA-DRB1 ChainsHumansImmune ToleranceMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicReceptors, ImmunologicCol2a1 protein, mouseCollagen Type IIHLA-DRB1*01:01 antigenHLA-DRB1 Chainsleukocyte-associated immunoglobulin-like receptor 1Receptors, Immunologic

Identifiers

PMID28887430
PMCPMC5714324
OpenAlexW2751046806

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.