ArticleActa neuropathologica2017
Bystander mechanism for complement-initiated early oligodendrocyte injury in neuromyelitis optica.
Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- Aquaporin-4 deficiency induced white matter injury via upregulated complement component 3 in cerebral small vessel disease.Journal of neuroinflammation · 2026Article
- Predict disabling severe attacks in neuromyelitis optica spectrum disorders: warning symptoms and innovative machine learning models.Journal of translational medicine · 2025Article
- Effect of L-Carnitine Level on the Risk of Neuromyelitis Optica Spectrum Disorders: A Two-Sample Mendelian Randomization Study.Molecular neurobiology · 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
- The Different Immune Response Between Onset and Remission of AQP4 Antibody-Positive Optic Neuritis Based on RNA Sequencing of Whole Blood.Journal of inflammation research · 2025Article
- Oligodendroglia in Neuromyelitis Optica Spectrum Disorder.Advances in neurobiology · 2025Review
- Complement updates in optic neuritis.Frontiers in neurology · 2025Review
- Serum LDL Promotes Microglial Activation and Exacerbates Demyelinating Injury in Neuromyelitis Optica Spectrum Disorder.Neuroscience bulletin · 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
- Pathogenic myelin-specific antibodies in multiple sclerosis target conformational proteolipid protein 1-anchored membrane domains.The Journal of clinical investigation · 2023Article
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
- ACT001 Relieves NMOSD Symptoms by Reducing Astrocyte Damage with an Autoimmune Antibody.Molecules (Basel, Switzerland) · 2023Article
- More Efficient Complement Activation by Anti-Aquaporin-4 Compared With Anti-Myelin Oligodendrocyte Glycoprotein Antibodies.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Astrocyte polarization in glaucoma: a new opportunity.Neural regeneration research · 2022Review
- Neutrophils activated by membrane attack complexes increase the permeability of melanoma blood vessels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Sera of Neuromyelitis Optica Patients Increase BID-Mediated Apoptosis in Astrocytes.International journal of molecular sciences · 2022Article
- A new form of axonal pathology in a spinal model of neuromyelitis optica.Brain : a journal of neurology · 2022Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Aquaporin-4 in Neuromyelitis Optica Spectrum Disorders: A Target of Autoimmunity in the Central Nervous System.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neuromyelitis optica spectrum disorder (herein called NMO) is an autoimmune inflammatory disease of the central nervous system in which immunoglobulin G antibodies against astrocyte water channel aquaporin-4 (AQP4-IgG) cause demyelination and neurological deficit. Injury to oligodendrocytes, which do not express AQP4, links the initiating pathogenic event of AQP4-IgG binding to astrocyte AQP4 to demyelination. Here, we report evidence for a complement 'bystander mechanism' to account for early oligodendrocyte injury in NMO in which activated, soluble complement proteins following AQP4-IgG binding to astrocyte AQP4 result in deposition of the complement membrane attack complex (MAC) on nearby oligodendrocytes. Primary cocultures of rat astrocytes and mature oligodendrocytes exposed to AQP4-IgG and complement showed early death of oligodendrocytes in close contact with astrocytes, which was not seen in pure oligodendrocyte cultures, in cocultures exposed to AQP4-IgG and C6-depleted serum, or when astrocytes were damaged by a complement-independent mechanism. Astrocyte-oligodendrocyte cocultures exposed to AQP4-IgG and complement showed prominent MAC deposition on oligodendrocytes in contact with astrocytes, whereas C1q, the initiating protein in the classical complement pathway, and C3d, a component of the alternative complement pathway, were deposited only on astrocytes. Early oligodendrocyte injury with MAC deposition was also found in rat brain following intracerebral injection of AQP4-IgG, complement and a fixable dead-cell stain. These results support a novel complement bystander mechanism for early oligodendrocyte injury and demyelination in NMO.
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Registered trials
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