ArticleNeuroscience bulletin2019
Myelin Oligodendrocyte Glycoprotein-IgG Contributes to Oligodendrocytopathy in the Presence of Complement, Distinct from Astrocytopathy Induced by AQP4-IgG.
Article in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Myelin oligodendrocyte glycoprotein antibody-associated isolated seizures in children: a retrospective single-center case series.Frontiers in immunology · 2026Article
- Efgartigimod for acute attacks of brainstem MOGAD followed by mycophenolate mofetil maintenance: a case report.Frontiers in immunology · 2026Article
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- FLAMES overlaying anti-N-methyl-D-aspartate receptor encephalitis: a case report and literature review.BMC neurology · 2024Review
- Evolution in anti-myelin oligodendrocyte glycoprotein antibody detection and its clinical significance: a narrative review.Annals of translational medicine · 2023Review
- Plasma Complement 3 and Complement 4 Are Promising Biomarkers for Distinguishing NMOSD From MOGAD and Are Associated With the Blood-Brain-Barrier Disruption in NMOSD.Frontiers in immunology · 2022Observational
- Treatment of MOG antibody associated disorders: results of an international survey.Journal of neurology · 2020Article
- Precision Medicine in Neurology: The Inspirational Paradigm of Complement Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Monoclonal Antibody-Based Treatments for Neuromyelitis Optica Spectrum Disorders: From Bench to Bedside.Neuroscience bulletin · 2020Review
- HLA association in MOG-IgG- and AQP4-IgG-related disorders of the CNS in the Dutch population.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin G against myelin oligodendrocyte glycoprotein (MOG-IgG) is detectable in neuromyelitis optica spectrum disorder (NMOSD) without aquaporin-4 IgG (AQP4-IgG), but its pathogenicity remains unclear. In this study, we explored the pathogenic mechanisms of MOG-IgG in vitro and in vivo and compared them with those of AQP4-IgG. MOG-IgG-positive serum induced complement activation and cell death in human embryonic kidney (HEK)-293T cells transfected with human MOG. In C57BL/6 mice and Sprague-Dawley rats, MOG-IgG only caused lesions in the presence of complement. Interestingly, AQP4-IgG induced astroglial damage, while MOG-IgG mainly caused myelin loss. MOG-IgG also induced astrocyte damage in mouse brains in the presence of complement. Importantly, we also observed ultrastructural changes induced by MOG-IgG and AQP4-IgG. These findings suggest that MOG-IgG directly mediates cell death by activating complement in vitro and producing NMOSD-like lesions in vivo. AQP4-IgG directly targets astrocytes, while MOG-IgG mainly damages oligodendrocytes.
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Registered trials
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.