ArticleAnnals of neurology2011
Ex vivo spinal cord slice model of neuromyelitis optica reveals novel immunopathogenic mechanisms.
Article in Annals of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 167 citations in OpenAlex.
- The IL-1β-STING Signaling Axis Drives Neuromyelitis Optica Pathogenesis in a Murine Model.Annals of neurology · 2026Article
- Targeting C3aR/STAT3 signaling attenuates neuroinflammation and reverses neurological impairment in Neuromyelitis optica.Fundamental research · 2026Article
- Neutrophil extracellular traps exacerbate blood-brain barrier disruption in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2026Article
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- Granulocyte and astrocyte markers distinguish MOG-antibody disease and neuromyelitis optica from multiple sclerosis.Brain : a journal of neurology · 2026Observational
- IL-1β contributes to neurological disability in NMOSD AQP4 + Patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Article
- Pilot Exploration of RGMa-BMP4 Signaling in Neutrophil Activation in NMOSD: Integrating Clinical and Molecular Insights.Molecular neurobiology · 2025Article
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
- Anterograde and trans-synaptic neurodegeneration in aquaporin-4-antibody neuromyelitis optica spectrum disorder patients with a history of transverse myelitis.Brain communications · 2025Article
- Complement activation in immunological neurological disorders: mechanisms and therapeutic strategies.Frontiers in neurology · 2025Review
- Decoding paraneoplastic neuromyelitis optica: a multi-omics investigation of tumor-driven T and B cell dynamics.Frontiers in immunology · 2025Review
- The Role of Gut Microbiota in Neuromyelitis Optica Spectrum Disorder.International journal of molecular sciences · 2024Review
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- Inhibition of complement C3 signaling ameliorates locomotor and visual dysfunction in autoimmune inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Granulocyte activation markers in cerebrospinal fluid differentiate acute neuromyelitis spectrum disorder from multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2023Article
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
- A novel aquaporin-4-associated optic neuritis rat model with severe pathological and functional manifestations.Journal of neuroinflammation · 2022Article
- Impaired response of blood neutrophils to cell-death stimulus differentiates AQP4-IgG-seropositive NMOSD from MOGAD.Journal of neuroinflammation · 2022Article
- Optic Neuritis in Multiple Sclerosis-A Review of Molecular Mechanisms Involved in the Degenerative Process.Current issues in molecular biology · 2022Review
41 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveNeuromyelitis optica (NMO) is a neuroinflammatory disease of spinal cord and optic nerve associated with serum autoantibodies (NMO-immunoglobulin G [IgG]) against astrocyte water channel aquaporin-4 (AQP4). Recent studies suggest that AQP4 autoantibodies are pathogenic. The objectives of this study were to establish an ex vivo spinal cord slice model in which NMO-IgG exposure produces lesions with characteristic NMO pathology, and to test the involvement of specific inflammatory cell types and soluble factors.
methodsVibratome-cut transverse spinal cord slices were cultured on transwell porous supports. After 7 days in culture, spinal cord slices were exposed to NMO-IgG and complement for 1 to 3 days. In some studies inflammatory cells or factors were added. Slices were examined for glial fibrillary acidic protein (GFAP), AQP4, and myelin immunoreactivity.
resultsSpinal cord cellular structure, including astrocytes, microglia, neurons, and myelin, was preserved in culture. NMO-IgG bound strongly to astrocytes in the spinal cord slices. Slices exposed to NMO-IgG and complement showed marked loss of GFAP, AQP4, and myelin. Lesions were not seen in the absence of complement or in spinal cord slices from AQP4 null mice. In cultures treated with submaximal NMO-IgG, the severity of NMO lesions was increased with inclusion of neutrophils, natural killer cells, or macrophages, or the soluble factors tumor necrosis factor α (TNFα), interleukin-6 (IL-6), IL-1β, or interferon-γ. Lesions were also produced in ex vivo optic nerve and hippocampal slice cultures.
interpretationThese results provide evidence for AQP4, complement- and NMO-IgG-dependent NMO pathogenesis in spinal cord, and implicate the involvement of specific immune cells and cytokines. Our ex vivo model allows for direct manipulation of putative effectors of NMO disease pathogenesis in a disease-relevant tissue.
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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.