ArticleFrontiers in neuroscience2023
Complement-dependent cytotoxicity of human autoantibodies against myelin oligodendrocyte glycoprotein.
Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 15 citations in OpenAlex.
- Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.Annals of clinical and translational neurology · 2026Article
- Serum and CSF cytokine profile impact clinical phenotype in pediatric MOGAD.Journal of neuroinflammation · 2026Article
- Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.Acta neuropathologica · 2026Article
- Life-Threatening SARS-CoV-2-Associated Encephalopathy and Multiorgan Failure in Children, Asia and Oceania, 2022-2024.Emerging infectious diseases · 2026Review
- Eculizumab treatment in the salvage therapy of MOGAD: a case report.Frontiers in immunology · 2026Article
- Investigation of anti-N-methyl-D-aspartate receptor and anti-myelin oligodendrocyte glycoprotein antibodies in patients with human herpesviruses-associated central nervous system infections.Journal of neurovirology · 2025Article
- Comparative evaluation of E. coli expression systems for soluble hScFv-IL-17A with an unpaired CDR-L3 cysteine.Journal, genetic engineering & biotechnology · 2025Article
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
- Complement Activation Profiles Predict Clinical Outcomes in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Translational insights from EAE models : decoding MOGAD pathogenesis and therapeutic innovation.Frontiers in immunology · 2025Review
- Different Complement Activation Patterns Following C5 Cleavage in MOGAD and AQP4-IgG+NMOSD.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Updates in NMOSD and MOGAD Diagnosis and Treatment: A Tale of Two Central Nervous System Autoimmune Inflammatory Disorders.Neurologic clinics · 2024Review
- Expression of CREBBP and EP300 Associated With Tumor Volume in Patients With Grade-3 Glioma: A Retrospective Analysis.Clinical Medicine Insights. Oncology · 2024Article
- MOGAD patient autoantibodies induce complement, phagocytosis, and cellular cytotoxicity.JCI insight · 2023Article
- Pathology of myelin oligodendrocyte glycoprotein antibody-associated disease: a comparison with multiple sclerosis and aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders.Frontiers in neurology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The autoantibody to myelin oligodendrocyte glycoprotein (MOG), a component of the central nervous system myelin, has been identified in a subset of demyelinating diseases. However, there is no convincing evidence to support the direct pathogenic contribution of this autoantibody. Objective: To elucidate the role of anti-MOG autoantibodies in human demyelinating disorders, we assessed the effect of autoantibodies on MOG-expressing cells. Methods: Mammalian cells expressing the human MOG protein reacted with human anti-MOG autoantibodies in the presence or absence of complement. Sera from 86 patients and 11 healthy sera were used. We analyzed anti-MOG antibody titers, IgG subclass, and their cytotoxic ability in sera from patients with various neurological diseases. Membrane attack complex (MAC) formation was examined by detection of complement C9 or C9neo with western blot or flow cytometry. Results: Among 86 patients, 40 were determined to be MOG-IgG-positive and 46 were negative. Anti-MOG-positive sera, but not -negative sera, caused cell death in MOG-expressing cells. This cytotoxic effect was disappeared after heat inactivation of sera. Importantly, anti-MOG IgG and externally added complement were necessary for sufficient cytotoxic effects. Anti-MOG autoantibodies were histologically colocalized with complement and formed a membrane attack complex consisting of anti-MOG IgG and complement factors. Conclusion: The human MOG antibody specifically killed MOG-expressing cells
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