ArticleProceedings of the National Academy of Sciences of the United States of America2006
Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in multiple sclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.
- The Elusive B Cell Antigen in Multiple Sclerosis: Time to Rethink CNS B Cell Functions.International journal of molecular sciences · 2025Pooled it
- DCIR-mediated inhibitory regulation of TLR7-MyD88 axis prevents autoimmune neuroinflammation.iScience · 2026Article
- Translational insights from EAE models : decoding MOGAD pathogenesis and therapeutic innovation.Frontiers in immunology · 2025Review
- The pathogenesis of multiple sclerosis: a series of unfortunate events.Clinical and experimental immunology · 2023Article
- Humoral signatures of MOG-antibody-associated disease track with age and disease activity.Cell reports. Medicine · 2023Article
- Complement-dependent cytotoxicity of human autoantibodies against myelin oligodendrocyte glycoprotein.Frontiers in neuroscience · 2023Article
- Application of optogenetic glial cells to neuron-glial communication.Frontiers in cellular neuroscience · 2023Review
- P2R Inhibitors Prevent Antibody-Mediated Complement Activation in an Animal Model of Neuromyelitis Optica : P2R Inhibitors Prevent Autoantibody Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Viral Membrane Fusion Proteins and RNA Sorting Mechanisms for the Molecular Delivery by Exosomes.Cells · 2021Review
- Adult onset acute disseminated encephalomyelitis: A case report.Radiology case reports · 2021Article
- A morphological analysis of activity-dependent myelination and myelin injury in transitional oligodendrocytes.Scientific reports · 2021Article
- Selective Depletion of Antigen-Specific Antibodies for the Treatment of Demyelinating Disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Cell-based assays for the detection of MOG antibodies: a comparative study.Journal of neurology · 2020Article
- HLA association in MOG-IgG- and AQP4-IgG-related disorders of the CNS in the Dutch population.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- Epstein-Barr Virus and Multiple Sclerosis.Frontiers in immunology · 2020Review
- B cells in autoimmune and neurodegenerative central nervous system diseases.Nature reviews. Neuroscience · 2019Review
- Myelin Oligodendrocyte Glycoprotein-IgG Contributes to Oligodendrocytopathy in the Presence of Complement, Distinct from Astrocytopathy Induced by AQP4-IgG.Neuroscience bulletin · 2019Article
- The role of B cells in multiple sclerosis: Current and future therapies.Cellular immunology · 2019Review
- The contribution of astrocytes to the neuroinflammatory response in multiple sclerosis and experimental autoimmune encephalomyelitis.Acta neuropathologica · 2019Review
- The Multiple Roles of B Cells in Multiple Sclerosis and Their Implications in Multiple Sclerosis Therapies.Cold Spring Harbor perspectives in medicine · 2019Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Although the cause of MS is still uncertain, many findings point toward an ongoing autoimmune response to myelin antigens. Because of its location on the outer surface of the myelin sheath and its pathogenicity in the experimental autoimmune encephalomyelitis model, myelin oligodendrocyte glycoprotein (MOG) is one of the potential disease-causing self antigens in MS. However, the role of MOG in the pathogenesis of MS has remained controversial. In this study we addressed the occurrence of autoantibodies to native MOG and its implication for demyelination and axonal loss in MS. We applied a high-sensitivity bioassay, which allowed detecting autoantibodies that bind to the extracellular part of native MOG. Antibodies, mostly IgG, were found in sera that bound with high affinity to strictly conformational epitopes of the extracellular domain of MOG. IgG but not IgM antibody titers to native MOG were significantly higher in MS patients compared with different control groups with the highest prevalence in primary progressive MS patients. Serum autoantibodies to native MOG induced death of MOG-expressing target cells in vitro. Serum from MS patients with high anti-MOG antibody titers stained white matter myelin in rat brain and enhanced demyelination and axonal damage when transferred to autoimmune encephalomyelitis animals. Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients.
Indexed as
Identifiers
What OpenQuestion holds
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.