ArticleJournal of neuroinflammation2024
CCR5-overexpressing mesenchymal stem cells protect against experimental autoimmune uveitis: insights from single-cell transcriptome analysis.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Zeb2 Controls Retinal Physiological and Pathological Angiogenesis by Regulating Astrocyte Proliferation and Differentiation.Cell proliferation · 2026Article
- The Advance of Single-Cell RNA Sequencing Applications in Ocular Physiology and Disease Research.Biomolecules · 2025Review
- Foxn3 is required to suppress aberrant ciliogenesis in nonphotoreceptor retinal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Potential therapeutic applications of stem cells in animal models of ocular affections.Inflammation and regeneration · 2025Review
- Comparative models of uveitis.Eye (London, England) · 2025Review
- Increasing robustness ofRegenerative therapy · 2025Article
- Mesenchymal Stromal Cell-Based Therapy: A Promising Approach for Autoimmune Diseases.Clinical reviews in allergy & immunology · 2025Review
- Differential Expression of ARG1 and MRC2 in Retinal Müller Glial Cells During Autoimmune Uveitis.Biomolecules · 2025Article
- Recent advances in the role of mesenchymal stem cells as modulators in autoinflammatory diseases.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Autoimmune uveitis is a leading cause of severe vision loss, and animal models provide unique opportunities for studying its pathogenesis and therapeutic strategies. Here we employ scRNA-seq, RNA-seq and various molecular and cellular approaches to characterize mouse models of classical experimental autoimmune uveitis (EAU), revealing that EAU causes broad retinal neuron degeneration and marker downregulation, and that Müller glia may act as antigen-presenting cells. Moreover, EAU immune response is primarily driven by Th1 cells, and results in dramatic upregulation of CC chemokines, especially CCL5, in the EAU retina. Accordingly, overexpression of CCR5, a CCL5 receptor, in mesenchymal stem cells (MSCs) enhances their homing capacity and improves their immunomodulatory outcomes in preventing EAU, by reducing infiltrating T cells and activated microglia and suppressing Nlrp3 inflammasome activation. Taken together, our data not only provide valuable insights into the molecular characteristics of EAU but also open an avenue for innovative MSC-based therapy.
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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.