ArticleJournal of neuroinflammation2018
Complement-dependent bystander injury to neurons in AQP4-IgG seropositive neuromyelitis optica.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
- Diagnostic Utility of Novel and Established Spinal MRI Signs in AQP4-IgG-Seropositive NMOSD Myelitis.Neurology · 2026Article
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Ferritin-ApoE nanocarrier for targeted therapy of neuromyelitis optica spectrum disorder in mice.Journal of neuroinflammation · 2026Article
- AQP4-IgG-Induced Astrocyte-Derived Small Extracellular Vesicles Carrying Mitochondrial DNA Regulate the TLR9/MyD88/NF-κB Pathway to Drive Microglial Activation and Neuromyelitis Optica.Neurochemical research · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Stem cell-derived extracellular vesicles as immunomodulatory agents: targeting pathological crosstalk in systemic lupus erythematosus and multiple sclerosis.Frontiers in medicine · 2026Review
- Cerebrospinal 14-3-3 Protein Levels as a Neuroaxonal Biomarker in Aquaporin-4 Antibody-Positive Neuromyelitis Optica Spectrum Disorder.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Complement inhibition rapidly blocks lesion extension and facilitates remyelination in neuromyelitis optica.Acta neuropathologica communications · 2025Article
- Efficacy of human umbilical cord mesenchymal stem cell in the treatment of neuromyelitis optica spectrum disorders: an animal study.Stem cell research & therapy · 2025Article
- Oligodendroglia in Neuromyelitis Optica Spectrum Disorder.Advances in neurobiology · 2025Review
- Involvement of Complement in Alzheimer's Disease: From Genetics Through Pathology to Therapeutic Strategies.Current topics in behavioral neurosciences · 2025Review
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
- Identification of potential biomarkers for neuromyelitis optica by quantitative proteomics.Annals of clinical and translational neurology · 2024Article
- Interferon-γ controls aquaporin 4-specific Th17 and B cells in neuromyelitis optica spectrum disorder.Brain : a journal of neurology · 2024Article
- Inflammatory Demyelinating Diseases of the Central Nervous System.Advances in neurobiology · 2024Review
- Regional spinal cord volumes and pain profiles in AQP4-IgG + NMOSD and MOGAD.Frontiers in neurology · 2024Article
- Pathogenic myelin-specific antibodies in multiple sclerosis target conformational proteolipid protein 1-anchored membrane domains.The Journal of clinical investigation · 2023Article
- A Clinical Approach to Existing and Emerging Therapeutics in Neuromyelitis Optica Spectrum Disorder.Current neurology and neuroscience reports · 2023Review
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAquaporin-4-immunoglobulin G (AQP4-IgG) seropositive neuromyelitis optica spectrum disorder (herein called NMO) is an autoimmune disease of the central nervous system in which AQP4-IgG binding to AQP4 on astrocytes results in complement-dependent astrocyte injury and secondary inflammation, demyelination, and neuron loss. We previously reported evidence for a complement bystander mechanism for early oligodendrocyte injury in NMO. Herein, we tested the hypothesis that complement bystander injury, which involves diffusion to nearby cells of activated soluble complement components from complement-injured astrocytes, is a general phenomenon that may contribute to neuronal injury in NMO.
methodsPrimary cocultures of rat astrocytes and cortical neurons were established to study complement-dependent cell death after exposure to AQP4-IgG and complement. In animal experiments, AQP4-IgG was delivered to adult rats by intracerebral injection. Cell cultures and rat brain were studied by immunofluorescence.
resultsIn primary astrocyte-neuron cocultures, addition of AQP4-IgG and complement resulted in death of neurons nearby astrocytes. Deposition of complement membrane attack complex C5b-9 was seen on neurons nearby astrocytes, whereas C1q, the initiating protein in the complement pathway, was seen only on astrocytes. Neuron death was not seen with a complement inhibitor, with C1q- or C6-depleted complement, in pure neuron cultures exposed to AQP4-IgG and complement or in cocultures exposed to an astrocyte toxin. Intracerebral injection in rats of AQP4-IgG and a fixable dead cell fluorescent marker produced death of neurons near astrocytes, with C5b-9 deposition. Neuron death was not seen in rats receiving a complement inhibitor or in AQP4-IgG-injected AQP4 knockout rats.
conclusionThese results support a novel mechanism for early neuron injury in NMO and provide evidence that complement bystander injury may be a general phenomenon for brain cell injury following AQP4-IgG-targeted astrocyte death.
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