ArticleRheumatology (Oxford, England)2025
Diminished SUV3 expression and its functional implications in the IFN-enriched monocyte subset of childhood Sjögren's disease.
Article in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 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.
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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
3 citing papers in PubMed.
- Mitochondrial RNA-Type I Interferon Axis in Sjögren's Disease: Molecular Mechanisms and Translational Implications.International journal of molecular sciences · 2026Review
- Asymmetric dimeric assembly of Suv3 helicase facilitates processive RNA unwinding.Nature communications · 2026Article
- High-resolution single-cell RNA sequencing using canFam4 reveals novel immune subsets and checkpoint programs in healthy dogs.Frontiers in immunology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
objectivesThis study investigates the molecular and functional implications of reduced Suv3-like RNA helicase (SUV3) expression in the interferon (IFN)-enriched subset of monocytes from childhood Sjögren's disease (cSjD). SUV3 is known to unwind double-stranded RNAs (dsRNAs) for homeostatic RNA decay within mitochondria.
methodsUsing single-cell RNA sequencing, we analysed highly inflammatory IFN-enriched CD14+ monocytes from cSjD patients. To model SUV3 deficiency, we performed SUV3 knockdown in monocytic cells and studied the origin, localization and accumulation of dsRNAs in the cytosol. Formaldehyde crosslinking immunoprecipitation (fCLIP)-qPCR identified an intracellular sensor of dsRNAs. We further examined patient monocytes using J2 anti-dsRNA antibodies and transmission electron microscopy (TEM) for subcellular localization. In vitro assays assessed the impact of SUV3 knockdown on oxidative stress, ATP production, migration and phagocytosis.
resultsSUV3 knockdown led to the accumulation of mitochondrial-dsRNAs (mt-dsRNAs) outside of the mitochondria, where they interacted with protein kinase R (PKR). This activated PKR, triggering a type I IFN signature and upregulating proinflammatory cytokines linked to fatigue. TEM revealed mt-dsRNAs in mitochondrial-derived vesicles and multi-vesicular bodies. Notably, cSjD monocytes had a significantly higher frequency of dsRNA-positive cells compared with controls (39% vs 0.08%, P < 0.002). SUV3 depletion also increased superoxide and ROS production, while impairing ATP synthesis, migration and phagocytosis, which are key innate immune functions. These defects were partially or fully reversed by co-knockdown of PKR.
conclusionSUV3 is the key driver for defective innate immune functions through mt-dsRNA-mediated PKR activation, which enhances cellular stress, mitochondrial dysfunction and inflammatory signatures, uncovering a novel mechanism in cSjD 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 Socratic graph.