NDLI: Altered signaling in systemic juvenile idiopathic arthritis monocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Macaubas, Claudia Wong, Elizabeth Zhang, Yujuan Nguyen, Khoa D. Lee, Justin Milojevic, Diana Shenoi, Susan Stevens, Anne M. Ilowite, Norman Saper, Vivian Lee, Tzielan Mellins, Elizabeth D.
Description	Country affiliation: United States Author Affiliation: Macaubas C ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Wong E ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Zhang Y ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Nguyen KD ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Lee J ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Milojevic D ( Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA.); Shenoi S ( Department of Pediatrics, Seattle Children's Hospital & University of Washington School of Medicine, Seattle, WA, USA.); Stevens AM ( Department of Pediatrics, Seattle Children's Hospital & University of Washington School of Medicine, Seattle, WA, USA.); Ilowite N ( Children's Hospital at Montefiore, Albert Einstein College of Medicine, Bronx, NY, USA.); Saper V ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Lee T ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA.); Mellins ED ( Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA, USA. Electronic address: mellins@stanford.edu.)
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 (IFN ) and type II (IFNÎ³) 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 IFNÎ³ hyporesponsive, but in treated, quiescent subjects, monocytes were hyperresponsive to IFNÎ³. 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.
File Format	HTM / HTML
ISSN	15216616
Volume Number	163
e-ISSN	15217035
Journal	Clinical Immunology
Language	English
Publisher	Elsevier
Publisher Date	2016-02-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Immunology Arthritis, Juvenile Genetics Interferons Metabolism Monocytes Stat1 Transcription Factor Suppressor Of Cytokine Signaling Proteins Adolescent Immunology Case-control Studies Child Child, Preschool Female Flow Cytometry Gene Expression Regulation Humans Infant Interferon-gamma Pharmacology Male Drug Effects Phosphorylation Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Young Adult Journal Article Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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