ArticleJournal of neuroinflammation2021
Astrocyte-specific expression of interleukin 23 leads to an aggravated phenotype and enhanced inflammatory response with B cell accumulation in the EAE model.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 32 citations in OpenAlex.
- Circulating miR-221/222 and Serum IL-23 in Treatment-Naïve Multiple Sclerosis: A Case-Control Study.Medicina (Kaunas, Lithuania) · 2026Observational
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- Mechanical compression induces neuronal apoptosis, reduces synaptic activity, and promotes glial neuroinflammation in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting the double-edged sword: cytokines in the pathogenesis and treatment of autoimmune diseases.Inflammopharmacology · 2025Review
- Generation and Characterization of Human iPSC-Derived Astrocytes with Potential for Modeling X-Linked Adrenoleukodystrophy Phenotypes.International journal of molecular sciences · 2025Article
- Article
- Identifying Diagnostic Markers and Constructing Predictive Models for Oxidative Stress in Multiple Sclerosis.International journal of molecular sciences · 2024Article
- IL-17A Facilitates Entry of Autoreactive T-Cells and Granulocytes into the CNS During EAE.Neuromolecular medicine · 2023Article
- RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis.Frontiers in molecular neuroscience · 2023Review
- MOG-Specific T Cells Lead to Spontaneous EAE with Multilocular B Cell Infiltration in the GF-IL23 Model.Neuromolecular medicine · 2022Article
- Chronic oligodendrocyte injury in central nervous system pathologies.Communications biology · 2022Review
- Single cell profiling of CD45Journal of neuroinflammation · 2022Article
- Isolation of Transcriptomic-Quality Total RNA from Mouse Spinal Cords.Current protocols · 2022Article
- Oligodendrocyte-Specific Deletion ofInternational journal of molecular sciences · 2021Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundInterleukin 23 is a critical cytokine in the pathogenesis of multiple sclerosis. But the local impact of interleukin 23 on the course of neuroinflammation is still not well defined. To further characterize the effect of interleukin 23 on CNS inflammation, we recently described a transgenic mouse model with astrocyte-specific expression of interleukin 23 (GF-IL23 mice). The GF-IL23 mice spontaneously develop a progressive ataxic phenotype with cerebellar tissue destruction and inflammatory infiltrates with high amounts of B cells most prominent in the subarachnoid and perivascular space.
methodsTo further elucidate the local impact of the CNS-specific interleukin 23 synthesis in autoimmune neuroinflammation, we induced a MOG35-55 experimental autoimmune encephalomyelitis (EAE) in GF-IL23 mice and WT mice and analyzed the mice by histology, flow cytometry, and transcriptome analysis.
resultsWe were able to demonstrate that local interleukin 23 production in the CNS leads to aggravation and chronification of the EAE course with a severe paraparesis and an ataxic phenotype. Moreover, enhanced multilocular neuroinflammation was present not only in the spinal cord, but also in the forebrain, brainstem, and predominantly in the cerebellum accompanied by persisting demyelination. Thereby, interleukin 23 creates a pronounced proinflammatory response with accumulation of leukocytes, in particular B cells, CD4+ cells, but also γδ T cells and activated microglia/macrophages. Furthermore, transcriptome analysis revealed an enhanced proinflammatory cytokine milieu with upregulation of lymphocyte activation markers, co-stimulatory markers, chemokines, and components of the complement system.
conclusionTaken together, the GF-IL23 model allowed a further breakdown of the different mechanisms how IL-23 drives neuroinflammation in the EAE model and proved to be a useful tool to further dissect the impact of interleukin 23 on neuroinflammatory models.
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