ArticleProceedings of the National Academy of Sciences of the United States of America2023
Dissection of complement and Fc-receptor-mediated pathomechanisms of autoantibodies to myelin oligodendrocyte glycoprotein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 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, 26 citations in OpenAlex.
- Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.Annals of clinical and translational neurology · 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
- Turncoat antibodies unmasked in a model of autoimmune demyelination: From biology to therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Outcomes After Acute Plasma Exchange for Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology · 2025Article
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
- Translational insights from EAE models : decoding MOGAD pathogenesis and therapeutic innovation.Frontiers in immunology · 2025Review
- Complement Activation Profiles Predict Clinical Outcomes in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Case Report: Fundus findings in myelin oligodendrocyte glycoprotein-associated optic neuritis.Frontiers in ophthalmology · 2025Article
- Acute ataxia in children: etiological spectrum and clinical characteristics.Frontiers in pediatrics · 2025Article
- NMOSD and MOGAD: an evolving disease spectrum.Nature reviews. Neurology · 2024Review
- Life history of a brain autoreactive T cell: From thymus through intestine to blood-brain barrier and brain lesion.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- MOG antibody-associated optic neuritis.Eye (London, England) · 2024Review
- Updates in NMOSD and MOGAD Diagnosis and Treatment: A Tale of Two Central Nervous System Autoimmune Inflammatory Disorders.Neurologic clinics · 2024Review
- A maternal high-fat diet during pregnancy and lactation induced depression-like behavior in offspring and myelin-related changes in the rat prefrontal cortex.Frontiers in molecular neuroscience · 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
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) have recently been established to define a new disease entity, MOG-antibody-associated disease (MOGAD), which is clinically overlapping with multiple sclerosis. MOG-specific antibodies (Abs) from patients are pathogenic, but the precise effector mechanisms are currently still unknown and no therapy is approved for MOGAD. Here, we determined the contributions of complement and Fc-receptor (FcR)-mediated effects in the pathogenicity of MOG-Abs. Starting from a recombinant anti-MOG (mAb) with human IgG1 Fc, we established MOG-specific mutant mAbs with differential FcR and C1q binding. We then applied selected mutants of this MOG-mAb in two animal models of experimental autoimmune encephalomyelitis. First, we found MOG-mAb-induced demyelination was mediated by both complement and FcRs about equally. Second, we found that MOG-Abs enhanced activation of cognate MOG-specific T cells in the central nervous system (CNS), which was dependent on FcR-, but not C1q-binding. The identification of complement-dependent and -independent pathomechanisms of MOG-Abs has implications for therapeutic strategies in MOGAD.
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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.