ArticleImmunology2016
MicroRNA223 promotes pathogenic T-cell development and autoimmune inflammation in central nervous system in mice.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MicroRNA Expression Profiles as Biomarkers of Response to Disease-Modifying Therapies in Multiple Sclerosis: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- From Demyelination to Intervention: Natural Compounds as Emerging Therapeutic Targets in Multiple Sclerosis Neuroinflammation.Journal of immunology research · 2026Review
- Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells.Journal of advanced research · 2025Article
- MicroRNAs in the biology and hallmarks of neurodegenerative diseases.Trends in molecular medicine · 2025Review
- Article
- Elevated NLRP3 Inflammasome Activation Is Associated with Motor Neuron Degeneration in ALS.Cells · 2024Article
- Time-resolved RNA signatures of CD4+ T cells in Parkinson's disease.Cell death discovery · 2023Article
- A panel of blood-based circulatory miRNAs with diagnostic potential in patients with psoriasis.Frontiers in medicine · 2023Article
- miRNA-Dependent CD4Multiple sclerosis international · 2021Review
- miR-223: An Effective Regulator of Immune Cell Differentiation and Inflammation.International journal of biological sciences · 2021Review
- MicroRNA 223 Targeting ATG16L1 Affects Microglial Autophagy in the Kainic Acid Model of Temporal Lobe Epilepsy.Frontiers in neurology · 2021Article
- Overexpression of miR-223 Promotes Tolerogenic Properties of Dendritic Cells Involved in Heart Transplantation Tolerance by Targeting Irak1.Frontiers in immunology · 2021Article
- miR-223: An Immune Regulator in Infectious Disorders.Frontiers in immunology · 2021Review
- GATA1/SP1 and miR-874 mediate enterovirus-71-induced apoptosis in a granzyme-B-dependent manner in Jurkat cells.Archives of virology · 2020Article
- MicroRNAs as disease progression biomarkers and therapeutic targets in experimental autoimmune encephalomyelitis model of multiple sclerosis.Neural regeneration research · 2020Review
- MiRNA-210 induces microglial activation and regulates microglia-mediated neuroinflammation in neonatal hypoxic-ischemic encephalopathy.Cellular & molecular immunology · 2020Article
- Potential for Targeting Myeloid Cells in Controlling CNS Inflammation.Frontiers in immunology · 2020Review
- Environmental Influencers, MicroRNA, and Multiple Sclerosis.Journal of central nervous system disease · 2020Review
- Osteoclastic microRNAs and their translational potential in skeletal diseases.Seminars in immunopathology · 2019Review
- MicroRNAs in brain development and cerebrovascular pathophysiology.American journal of physiology. Cell physiology · 2019Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an incurable central nervous system autoimmune disease. Understanding MS pathogenesis is essential for the development of new MS therapies. In the present study, we identified a novel microRNA (miR) that regulates experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Expression of miR223 was up-regulated specifically in spinal cords and lymphoid organs but not in other examined tissues. A global miR223 knockout (miR223(-/-) ) in mice led to a significant delay in EAE onset, reduction in spinal cord lesion, and lessening of neurological symptoms. These protective effects could be reproduced in bone marrow chimeras reconstituted with miR223(-/-) haematopoietic stem cells. We also found that miR223 deficiency reduced T helper type 1 (Th1) and Th17 infiltration into spinal cords. To address underlying mechanisms, we investigated the role of miR223 in regulating the function, development and interaction of the major immune cells. Expression of the genes associated with dendritic cell (DC) activation (CD86 and MHC II) and Th1 and Th17 differentiation [interleukin-12 (IL-12) and IL-23, respectively] was significantly decreased in the spleens of miR223(-/-) mice bearing EAE. The miR223(-/-) DCs expressed significantly lower levels of basal and lipopolysaccharide-induced IL-12 and IL-23 compared with the wild-type DCs. These data are consistent with the observed lower efficiency of miR223(-/-) DCs to support Th1 and Th17 differentiation from naive T cells over-expressing an EAE antigen-specific T-cell receptor. Our data suggest that miR223 promotes EAE, probably through enhancing DC activation and subsequently the differentiation of naive T cells toward Th1 and Th17 effector cells.
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Registered trials
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