Evidence map›Paper›PMID 30127787›Full record

ArticleFrontiers in immunology2018

T Cell Receptor-Independent, CD31/IL-17A-Driven Inflammatory Axis Shapes Synovitis in Juvenile Idiopathic Arthritis.

Ian D Ferguson, Patricia Griffin, Joshua J Michel, Hiroshi Yano, Sarah L Gaffen, Robert G Mueller, Jeffrey A Dvergsten, Jon D Piganelli, Margalit E Rosenkranz, Daniel A Kietz and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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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 4 institutions in 1 country.

Ian D FergusonDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Patricia GriffinDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Joshua J MichelDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Hiroshi YanoGraduate Program in Microbiology and Immunology School of Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Sarah L GaffenDepartment of Medicine, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, United States.
Robert G MuellerDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Jeffrey A DvergstenDepartment of Pediatrics, Duke University Medical Center, Durham, NC, United States.
Jon D PiganelliDepartment of Immunology, University of Pittsburgh, Pittsburgh, PA, United States.
Margalit E RosenkranzDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Daniel A KietzDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
Abbe N VallejoDepartment of Pediatrics, University of Pittsburgh, Pittsburgh, PA, United States.
University of Pittsburgh · USUniversity of Pittsburgh Medical Center · USChildren's Hospital of Pittsburgh · USDuke Medical Center · US

Funding

Negative Control of IL-17R Signaling: Implications for Fungal ImmunityR01AI107825 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2014 to 2018
$1.9M
PITTSBURGH PEDIATRIC RHEUMATOLOGY TRAINING GRANTT32AR052282 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2005 to 2014
$1.8M
NIAID NIH HHS R01 AI107825NIAMS NIH HHS T32 AR052282
6 · The paper itself

Abstract

T cells are considered autoimmune effectors in juvenile idiopathic arthritis (JIA), but the antigenic cause of arthritis remains elusive. Since T cells comprise a significant proportion of joint-infiltrating cells, we examined whether the environment in the joint could be shaped through the inflammatory activation by T cells that is independent of conventional TCR signaling. We focused on the analysis of synovial fluid (SF) collected from children with oligoarticular and rheumatoid factor-negative polyarticular JIA. Cytokine profiling of SF showed dominance of five molecules including IL-17A. Cytometric analysis of the same SF samples showed enrichment of αβT cells that lacked both CD4 and CD8 co-receptors [herein called double negative (DN) T cells] and also lacked the CD28 costimulatory receptor. However, these synovial αβT cells expressed high levels of CD31, an adhesion molecule that is normally employed by granulocytes when they transit to sites of injury. In receptor crosslinking assays, ligation of CD31 alone on synovial CD28

Indexed as

Arthritis, JuvenileCD28 AntigensChildCohort StudiesCytokinesFemaleHumansInterleukin-17MaleMetalloporphyrinsOxidoreductasesPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Promoter Regions, GeneticProto-Oncogene Proteins c-ablReceptors, Antigen, T-CellCD28 AntigensCytokinesIL17A protein, humanInterleukin-17manganese (III) meso-tetrakis(N-ethylpyridinium-2-yl)porphyrinMetalloporphyrinsOxidoreductasesPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-ablReceptors, Antigen, T-CellCD31double negative alpha beta T cellsfibrocyte-like cellsIL-17juvenile idiopathic arthritisoxidoreductasesynovial inflammationTCR-independent

Identifiers

PMID30127787
PMCPMC6087740
OpenAlexW2885152383

What OpenQuestion holds

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Registered trials

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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.