ArticleThe Journal of clinical investigation2022
microRNA-92a promotes CNS autoimmunity by modulating the regulatory and inflammatory T cell balance.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- A microRNA atlas of CD4+ T cell subsets in experimental autoimmune encephalomyelitis identifies regulators of disease pathogenesis.PLoS biology · 2026Article
- Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026Review
- Pathology-directed drug delivery strategies: How to overcome blood-brain barrier for the treatment of brain diseases.Acta pharmaceutica Sinica. B · 2026Review
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- Mapping the Evolution of Experimental Autoimmune Encephalomyelitis Research (2000-2024): A Global Bibliometric and Knowledge Domain Analysis.Molecular neurobiology · 2026Review
- Article
- T cell-mediated immunodysregulation in multiple sclerosis: from pathogenic subsets to therapeutic advances.Frontiers in immunology · 2026Review
- Regulatory T cells promote microglia-mediated synapse engulfment and functional recovery via the OPN-CD74 axis after spinal cord injury in mice.Journal of neuroinflammation · 2025Article
- MicroRNAs in the biology and hallmarks of neurodegenerative diseases.Trends in molecular medicine · 2025Review
- Immunomodulatory Role of Mesenchymal Stem Cell Therapy in Multiple Sclerosis: A Systematic Review.Cureus · 2025Review
- Cell culture expansion media choice affects secretory, protective and immuno-modulatory features of adipose mesenchymal stromal cell-derived secretomes for orthopaedic applications.Regenerative therapy · 2025Article
- Article
- Interacting roles of gut microbiota and T cells in the development of autoimmune hepatitis.Frontiers in immunology · 2025Review
- The Potential of Mesenchymal Stem Cells in Treating Spinocerebellar Ataxia: Advances and Future Directions.Biomedicines · 2024Review
- Infiltrating treg reprogramming in the tumor immune microenvironment and its optimization for immunotherapy.Biomarker research · 2024Review
- Re-establishing immune tolerance in multiple sclerosis: focusing on novel mechanisms of mesenchymal stem cell regulation of Th17/Treg balance.Journal of translational medicine · 2024Review
- Profiling Small RNA From Brain Extracellular Vesicles in Individuals With Depression.The international journal of neuropsychopharmacology · 2024Article
- Regulatory T cells promote functional recovery after spinal cord injury by alleviating microglia inflammation via STAT3 inhibition.CNS neuroscience & therapeutics · 2023Article
- Emerging imaging and liquid biomarkers in multiple sclerosis.European journal of immunology · 2023Review
- Erythrocyte miRNA-92a-3p interactions with PfEMP1 as determinants of clinical malaria.Functional & integrative genomics · 2023Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
A disequilibrium between immunosuppressive Tregs and inflammatory IL-17-producing Th17 cells is a hallmark of autoimmune diseases, including multiple sclerosis (MS). However, the molecular mechanisms underlying the Treg and Th17 imbalance in CNS autoimmunity remain largely unclear. Identifying the factors that drive this imbalance is of high clinical interest. Here, we report a major disease-promoting role for microRNA-92a (miR-92a) in CNS autoimmunity. miR-92a was elevated in experimental autoimmune encephalomyelitis (EAE), and its loss attenuated EAE. Mechanistically, miR-92a mediated EAE susceptibility in a T cell-intrinsic manner by restricting Treg induction and suppressive capacity, while supporting Th17 responses, by directly repressing the transcription factor Foxo1. Although miR-92a did not directly alter Th1 differentiation, it appeared to indirectly promote Th1 cells by inhibiting Treg responses. Correspondingly, miR-92a inhibitor therapy ameliorated EAE by concomitantly boosting Treg responses and dampening inflammatory T cell responses. Analogous to our findings in mice, miR-92a was elevated in CD4+ T cells from patients with MS, and miR-92a silencing in patients' T cells promoted Treg development but limited Th17 differentiation. Together, our results demonstrate that miR-92a drives CNS autoimmunity by sustaining the Treg/Th17 imbalance and implicate miR-92a as a potential therapeutic target for MS.
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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.