ArticleJCI insight2023
MOGAD patient autoantibodies induce complement, phagocytosis, and cellular cytotoxicity.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed.
- Pathogenic properties of myasthenia gravis AChR autoantibodies associate with clinical response to efgartigimod.Journal of neurology, neurosurgery, and psychiatry · 2026Trial
- BCMA-directed mRNA CAR-T cell therapy for myasthenia gravis: exploratory biomarker analysis of a placebo-controlled phase 2b trial.Nature medicine · 2026Trial
- Identification of risk factors for relapse at initial onset in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis using ophthalmic findings.Japanese journal of ophthalmology · 2026Article
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Immuno-Proteomic Features Associated to Relapse Risk in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Serum and CSF cytokine profile impact clinical phenotype in pediatric MOGAD.Journal of neuroinflammation · 2026Article
- The human IG heavy chain constant gene locus is enriched for large structural variants and coding polymorphisms that vary among human populations.Cell genomics · 2026Article
- Patient-Derived Monoclonal Myelin Oligodendrocyte Glycoprotein Autoantibodies Mediate Cytotoxicity.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Anti-MOG IgG in EAE models clinical aspects of pediatric MOGAD.Frontiers in immunology · 2026Article
- Eculizumab treatment in the salvage therapy of MOGAD: a case report.Frontiers in immunology · 2026Article
- MOG IgG3-Subclass Antibodies in MOG-Associated Disease: Insights From a Pediatric Case With IgG1 Deficiency and Literature Review.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- Inflammatory transcriptomic signatures in a human cellular NMOSD model reveal upregulation of NF-κB and IL6 pathways.Scientific reports · 2025Article
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- MOGAD: A Shifting Landscape-From Pathogenesis to Personalised Management, Global Perspectives and Latin American Insights.Biomedicines · 2025Review
- Outcomes After Acute Plasma Exchange for Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology · 2025Article
- Diversity, Functional Complexity, and Translational Potential of Glial Cells in the Central Nervous System.International journal of molecular sciences · 2025Review
- The human IG heavy chain constant gene locus is enriched for large structural variants and coding polymorphisms that vary among human populations.bioRxiv : the preprint server for biology · 2025Article
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
- Serum sEV miRNAs as Biomarkers in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Molecular neurobiology · 2025Article
- AChR Autoantibody Pathogenic Properties Are Heterogeneously Distributed and Undergo Temporal Changes Among Patients With Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an inflammatory demyelinating CNS condition characterized by the presence of MOG autoantibodies. We sought to investigate whether human MOG autoantibodies are capable of mediating damage to MOG-expressing cells through multiple mechanisms. We developed high-throughput assays to measure complement activity (CA), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and antibody-dependent cellular cytotoxicity (ADCC) of live MOG-expressing cells. MOGAD patient sera effectively mediate all of these effector functions. Our collective analyses reveal that (a) cytotoxicity is not incumbent on MOG autoantibody quantity alone; (b) engagement of effector functions by MOGAD patient serum is bimodal, with some sera exhibiting cytotoxic capacity while others did not; (c) the magnitude of CDC and ADCP is elevated closer to relapse, while MOG-IgG binding is not; and (d) all IgG subclasses can damage MOG-expressing cells. Histopathology from a representative MOGAD case revealed congruence between lesion histology and serum CDC and ADCP, and we identified NK cells, mediators of ADCC, in the cerebrospinal fluid of relapsing patients with MOGAD. Thus, MOGAD-derived autoantibodies are cytotoxic to MOG-expressing cells through multiple mechanisms, and assays quantifying CDC and ADCP may prove to be effective tools for predicting risk of future relapses.
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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 Socratic graph.