Evidence map›Paper›PMID 26747737›Full record

ArticleClinical immunology (Orlando, Fla.)2016

Altered signaling in systemic juvenile idiopathic arthritis monocytes.

Claudia Macaubas, Elizabeth Wong, Yujuan Zhang, Khoa D Nguyen, Justin Lee, Diana Milojevic, Susan Shenoi, Anne M Stevens, Norman Ilowite, Vivian Saper and 2 more

Abstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Type I Interferon-Driven Monocyte Dysregulation and MAS-associated CD8bioRxiv : the preprint server for biology · 2026
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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

12 authors at 4 institutions in 1 country.

Claudia MacaubasDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Elizabeth WongDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Yujuan ZhangDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Khoa D NguyenDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Justin LeeDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Diana MilojevicDepartment of Pediatrics, University of California San Francisco, San Francisco, CA, USA.
Susan ShenoiDepartment of Pediatrics, Seattle Children's Hospital & University of Washington School of Medicine, Seattle, WA, USA.
Anne M StevensDepartment of Pediatrics, Seattle Children's Hospital & University of Washington School of Medicine, Seattle, WA, USA.
Norman IlowiteChildren's Hospital at Montefiore, Albert Einstein College of Medicine, Bronx, NY, USA.
Vivian SaperDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Tzielan LeeDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.
Elizabeth D MellinsDepartment of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA. Electronic address: mellins@stanford.edu.
Stanford University · USSeattle Children's Hospital · USChildren's Hospital at Montefiore · USUniversity of California, San Francisco · US

Funding

Training Program in Adult and Pediatric RheumatologyT32AR050942 · NIAMS · STANFORD UNIVERSITY · PI LEWIS, DAVID BRAM, ROBINSON, WILLIAM H · 2005 to 2025
$6.6M
A role for IL-1 in SJIA monocyte phenotypes: A RAPPORT ancillary studyR01AR061297 · NIAMS · STANFORD UNIVERSITY · PI MELLINS, ELIZABETH D · 2010 to 2013
$1.2M
Immune cell dysfunction in SJIAR21AI075254 · NIAID · STANFORD UNIVERSITY · PI MELLINS, ELIZABETH D · 2008 to 2009
$435k
NIAID NIH HHS R21 AI075254NIAMS NIH HHS R01 AR061297NIAMS NIH HHS R01AR061297NIAMS NIH HHS T32 AR050942
6 · The paper itself

Abstract

Systemic juvenile idiopathic arthritis (sJIA) is characterized by systemic inflammation and arthritis. Monocytes are implicated in sJIA pathogenesis, but their role in disease is unclear. The response of sJIA monocytes to IFN may be dysregulated. We examined intracellular signaling in response to IFN type I (IFNα) and type II (IFNγ) in monocytes during sJIA activity and quiescence, in 2 patient groups. Independent of disease activity, monocytes from Group 1 (collected between 2002 and 2009) showed defective STAT1 phosphorylation downstream of IFNs, and expressed higher transcript levels of SOCS1, an inhibitor of IFN signaling. In the Group 2 (collected between 2011 and 2014), monocytes of patients with recent disease onset were IFNγ hyporesponsive, but in treated, quiescent subjects, monocytes were hyperresponsive to IFNγ. Recent changes in medication in sJIA may alter the IFN hyporesponsiveness. Impaired IFN/pSTAT1 signaling is consistent with skewing of sJIA monocytes away from an M1 phenotype and may contribute to disease pathology.

Indexed as

AdolescentArthritis, JuvenileCase-Control StudiesChildChild, PreschoolFemaleFlow CytometryGene Expression RegulationHumansInfantInterferon-gammaInterferonsMaleMonocytesPhosphorylationReal-Time Polymerase Chain ReactionInterferon-gammaInterferonsSOCS1 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsIFN signalingJuvenile arthritisMonocytesSOCS1

Identifiers

PMID26747737
PMCPMC4753112
OpenAlexW2227382780

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.