ArticlePloS one2016
TLR3 Agonist Poly-IC Induces IL-33 and Promotes Myelin Repair.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- The Role of Selected Interleukins in the Development and Progression of Multiple Sclerosis-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- The Role of the IL-33/ST2 Axis in Nervous System Development and Diseases.Immunology and cell biology · 2026Review
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- The IL-33/ST2 Axis Protects the Hippocampus from LPS-Induced Inflammation and Damage by Modulating Microglial Phenotype.Biomedicines · 2026Article
- Article
- Tropisetron Suppresses Chronic Pancreatitis and Pancreatic Cancer by Blocking Interleukin 33 Expression.Cancers · 2025Article
- Review
- Assessing the inflammation in pediatric MOGAD: Significance of CSF HMGB1 and related biomarkers.Frontiers in immunology · 2025Article
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- Impact of calcitriol and PGDDrug delivery and translational research · 2024Article
- Review
- Targeted proteomics of cerebrospinal fluid in treatment naïve multiple sclerosis patients identifies immune biomarkers of clinical phenotypes.Scientific reports · 2024Article
- Statin prevents cancer development in chronic inflammation by blocking interleukin 33 expression.Nature communications · 2024Article
- CNS Resident Innate Immune Cells: Guardians of CNS Homeostasis.International journal of molecular sciences · 2024Review
- Review
- Cause or consequence? The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases.Frontiers in immunology · 2023Article
- Article
- Host-Viral Interactions in the Pathogenesis of Ulcerative Colitis.International journal of molecular sciences · 2021Review
- Therapeutic Potential of Cytokines in Demyelinating Lesions After Stroke.Journal of molecular neuroscience : MN · 2021Review
- Vagal-α7nAChR signaling is required for lung anti-inflammatory responses and arginase 1 expression during an influenza infection.Acta pharmacologica Sinica · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImpaired remyelination of demyelinated axons is a major cause of neurological disability. In inflammatory demyelinating disease of the central nervous system (CNS), although remyelination does happen, it is often incomplete, resulting in poor clinical recovery. Poly-IC a known TLR3 agonist and IL-33, a cytokine which is induced by poly-IC are known to influence recovery and promote repair in experimental models of CNS demyelination. METHODOLOGY AND PRINCIPAL
findingsWe examined the effect of addition of poly-IC and IL-33 on the differentiation and maturation of oligodendrocyte precursor cells (OPC) cultured in vitro. Both Poly-IC and IL-33 induced transcription of myelin genes and the differentiation of OPC to mature myelin forming cells. Poly-IC induced IL-33 in OPC and addition of IL-33 to in vitro cultures, amplified further, IL-33 expression suggesting an autocrine regulation of IL-33. Poly-IC and IL-33 also induced phosphorylation of p38MAPK, a signaling molecule involved in myelination. Following the induction of gliotoxic injury with lysolecithin to the corpus callosum (CC), treatment of animals with poly-IC resulted in greater recruitment of OPC and increased staining for myelin in areas of demyelination. Also, poly-IC treated animals showed greater expression of IL-33 and higher expression of M2 phenotype macrophages in the CC. CONCLUSION/SIGNIFICANCE: Our studies suggest that poly-IC and IL-33 play a role in myelin repair by enhancing expression of myelin genes and are therefore attractive therapeutic agents for use as remyelinating agents in human demyelinating disease.
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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.