ArticleJCI insight2018
Dysregulated NK cell PLCγ2 signaling and activity in juvenile dermatomyositis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Psychometric properties of patient-reported outcomes measurement information system (PROMIS) fixed short forms in Juvenile Myositis.Seminars in arthritis and rheumatism · 2025Article
- Juvenile Dermatomyositis: Updates in Pathogenesis and Biomarkers, Current Treatment, and Emerging Targeted Therapies.Paediatric drugs · 2025Review
- Decreased Peripheral Blood Natural Killer Cell Count in Untreated Juvenile Dermatomyositis Is Associated with Muscle Weakness.International journal of molecular sciences · 2024Article
- Coordinated immune dysregulation in juvenile dermatomyositis revealed by single-cell genomics.JCI insight · 2024Article
- Mass cytometry: exploring the immune landscape of systemic autoimmune and inflammatory diseases in the past fourteen years.Frontiers in immunology · 2024Review
- Single-cell mass cytometry in immunological skin diseases.Frontiers in immunology · 2024Review
- Coordinated immune dysregulation in Juvenile Dermatomyositis revealed by single-cell genomics.bioRxiv : the preprint server for biology · 2023Article
- Expansion of a novel population of NK cells with low ribosome expression in juvenile dermatomyositis.Frontiers in immunology · 2022Article
- Multi-Modal Single-Cell Sequencing Identifies Cellular Immunophenotypes Associated With Juvenile Dermatomyositis Disease Activity.Frontiers in immunology · 2022Article
- MECHANISTIC AND DATA-DRIVEN MODELS OF CELL SIGNALING: TOOLS FOR FUNDAMENTAL DISCOVERY AND RATIONAL DESIGN OF THERAPY.Current opinion in systems biology · 2021Article
- Juvenile Dermatomyositis: New Clues to Diagnosis and Therapy.Current treatment options in rheumatology · 2021Article
- The Role of Immune Cells in the Pathogenesis of Idiopathic Inflammatory Myopathies.Aging and disease · 2021Review
- Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021Review
- Serum protein biomarkers for juvenile dermatomyositis: a pilot study.BMC rheumatology · 2020Article
- Advances Toward Precision Medicine in Juvenile Dermatomyositis.Current rheumatology reports · 2019Review
- Immunomics in Pediatric Rheumatic Diseases.Frontiers in medicine · 2019Review
- Exercise modulation of BDNF/TrkB signaling in Parkinson's disease: an evidence-calibrated review of neuroprotective mechanisms, biomarker limitations, and translational gaps.Frontiers in neurologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Juvenile dermatomyositis (JDM) is a debilitating pediatric autoimmune disease manifesting with characteristic rash and muscle weakness. To delineate signaling abnormalities in JDM, mass cytometry was performed with PBMCs from treatment-naive JDM patients and controls. NK cell percentages were lower while frequencies of naive B cells and naive CD4+ T cells were higher in JDM patients than in controls. These cell frequency differences were attenuated with cessation of active disease. A large number of signaling differences were identified in treatment-naive JDM patients compared with controls. Classification models incorporating feature selection demonstrated that differences in phospholipase Cγ2 (PLCγ2) phosphorylation comprised 10 of 12 features (i.e., phosphoprotein in a specific immune cell subset) distinguishing the 2 groups. Because NK cells represented 5 of these 12 features, further studies focused on the PLCγ2 pathway in NK cells, which is responsible for stimulating calcium flux and cytotoxic granule movement. No differences were detected in upstream signaling or total PLCγ2 protein levels. Hypophosphorylation of PLCγ2 and downstream mitogen-activated protein kinase-activated protein kinase 2 were partially attenuated with cessation of active disease. PLCγ2 hypophosphorylation in treatment-naive JDM patients resulted in decreased calcium flux. The identification of dysregulation of PLCγ2 phosphorylation and decreased calcium flux in NK cells provides potential mechanistic insight into JDM pathogenesis.
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Registered trials
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.