ArticleMediators of inflammation2013
Local overexpression of interleukin-11 in the central nervous system limits demyelination and enhances remyelination.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
- AAV-mediated delivery of a proliferation inducing ligand (APRIL) to cortical neurons limits inflammation and demyelination in the corpus callosum of the cuprizone mouse model.Journal of neuroinflammation · 2025Article
- How do different cell populations orchestrate myelin regeneration?Biochemical Society transactions · 2025Review
- Neuroinflammatory Proteins in Huntington's Disease: Insights into Mechanisms, Diagnosis, and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- An exhausted-like microglial population accumulates in aged and APOE4 genotype Alzheimer's brains.Immunity · 2024Article
- Understanding interleukin 11 as a disease gene and therapeutic target.The Biochemical journal · 2023Review
- Interleukin-11 in Pathologies of the Nervous System.Molecular biology · 2023Article
- IL11 Stimulates IL33 Expression and Proinflammatory Fibroblast Activation across Tissues.International journal of molecular sciences · 2022Article
- New insights into the immunologic role of oligodendrocyte lineage cells in demyelination diseases.Journal of biomedical research · 2022Article
- Uptake of Nanotitania by Gingival Epithelial Cells Promotes Inflammatory Response and Is Accelerated byInternational journal of molecular sciences · 2021Article
- Review
- Environmental Enrichment and Its Benefits for Migraine: Dendritic Cell Extracellular Vesicles as an Effective Mimetic.Journal of cellular immunology · 2021Article
- Cross-Talk of the CNS With Immune Cells and Functions in Health and Disease.Frontiers in neurology · 2021Review
- Assessment of ability of human adipose derived stem cells for long term overexpression of IL-11 and IL-13 as therapeutic cytokines.Cytotechnology · 2020Article
- GM2 ganglioside accumulation causes neuroinflammation and behavioral alterations in a mouse model of early onset Tay-Sachs disease.Journal of neuroinflammation · 2020Article
- Neuroprotective effects of ellagic acid on cuprizone-induced acute demyelination through limitation of microgliosis, adjustment of CXCL12/IL-17/IL-11 axis and restriction of mature oligodendrocytes apoptosis.Pharmaceutical biology · 2017Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Demyelination is one of the pathological hallmarks of multiple sclerosis (MS). To date, no therapy is available which directly potentiates endogenous remyelination. Interleukin-11 (IL-11), a member of the gp130 family of cytokines, is upregulated in MS lesions. Systemic IL-11 treatment was shown to ameliorate clinical symptoms in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. IL-11 modulates immune cells and protects oligodendrocytes in vitro. In this study, the cuprizone-induced demyelination mouse model was used to elucidate effects of IL-11 on de- and remyelination, independent of the immune response. Prophylactic-lentiviral- (LV-) mediated overexpression of IL-11 in mouse brain significantly limited acute demyelination, which was accompanied with the preservation of CC1(+) mature oligodendrocytes (OLs) and a decrease in microglial activation (Mac-2(+)). We further demonstrated that IL-11 directly reduces myelin phagocytosis in vitro. When IL-11 expressing LV was therapeutically applied in animals with extensive demyelination, a significant enhancement of remyelination was observed as demonstrated by Luxol Fast Blue staining and electron microscopy imaging. Our results indicate that IL-11 promotes maturation of NG2(+) OPCs into myelinating CC1(+) OLs and may thus explain the enhanced remyelination. Overall, we demonstrate that IL-11 is of therapeutic interest for MS and other demyelinating diseases by limiting demyelination and promoting remyelination.
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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.