ArticleJCI insight2023
Single-cell transcriptomics reveals variations in monocytes and Tregs between gout flare and remission.
Article in JCI insight, 2023. 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 28 papers.
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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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Who cites it
28 citing papers in PubMed, 31 citations in OpenAlex.
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- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
- ICAM signaling rewires the inflammatory communication network in pediatric gout.Frontiers in immunology · 2026Article
- Spatiotemporal immune gradients in gout: immune response-driven activation of the NLRP3-IL-1β axis and its transition to trained immunity.Frontiers in immunology · 2026Review
- Integrated multi-omics analysis of dampness-heat gout reveals diagnostic biomarkers and therapeutic targets.Frontiers in immunology · 2026Article
- From uric acid to tophi: multistage molecular and cellular mechanisms of tophi formation.Frontiers in immunology · 2026Review
- MSC administration resolves experimental acute gout increasing specialized pro-resolving mediators synthesis through a super-induction of prostaglandin EStem cell research & therapy · 2025Article
- Navigating the Autophagy Maze: ATG and Their Impact on Neurodegenerative Diseases.Molecular neurobiology · 2025Review
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- Research progress of non-coding RNA regulating the role of PANoptosis in diabetes mellitus and its complications.Apoptosis : an international journal on programmed cell death · 2025Review
- Purine metabolism-associated key genes depict the immune landscape in gout patients.Discover oncology · 2025Article
- Delineating circulating lymphocyte subsets in the transition from gout remission to recurrence.Frontiers in immunology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gout commonly manifests as a painful, self-limiting inflammatory arthritis. Nevertheless, the understanding of the inflammatory and immune responses underlying gout flares and remission remains ambiguous. Here, based on single-cell RNA-Seq and an independent validation cohort, we identified the potential mechanism of gout flare, which likely involves the upregulation of HLA-DQA1+ nonclassical monocytes and is related to antigen processing and presentation. Furthermore, Tregs also play an essential role in the suppressive capacity during gout remission. Cell communication analysis suggested the existence of altered crosstalk between monocytes and other T cell types, such as Tregs. Moreover, we observed the systemic upregulation of inflammatory and cytokine genes, primarily in classical monocytes, during gout flares. All monocyte subtypes showed increased arachidonic acid metabolic activity along with upregulation of prostaglandin-endoperoxide synthase 2 (PTGS2). We also detected a decrease in blood arachidonic acid and an increase in leukotriene B4 levels during gout flares. In summary, our study illustrates the distinctive immune cell responses and systemic inflammation patterns that characterize the transition from gout flares to remission, and it suggests that blood monocyte subtypes and Tregs are potential intervention targets for preventing recurrent gout attacks and progression.
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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.