ArticleProceedings of the National Academy of Sciences of the United States of America2006
Autoantibody-mediated demyelination depends on complement activation but not activatory Fc-receptors.
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 34 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders-A Systematic Review.Frontiers in immunology · 2018Pooled it
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Review
- Immunoglobulin G and Complement as Major Players in the Neurodegeneration of Multiple Sclerosis.Biomolecules · 2024Review
- Multiple sclerosis plasma IgG aggregates induce complement-dependent neuronal apoptosis.Cell death & disease · 2023Article
- The role of the complement system in Multiple Sclerosis: A review.Frontiers in immunology · 2022Review
- The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.Frontiers in molecular neuroscience · 2022Review
- Next-generation Bruton's tyrosine kinase inhibitor BIIB091 selectively and potently inhibits B cell and Fc receptor signaling and downstream functions in B cells and myeloid cells.Clinical & translational immunology · 2021Article
- Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis.Brain, behavior, and immunity · 2020Article
- Complement-Mediated Microglial Phagocytosis and Pathological Changes in the Development and Degeneration of the Visual System.Frontiers in immunology · 2020Review
- Review
- Immunopathological Factors Associated with Disability in Multiple Sclerosis.Noro psikiyatri arsivi · 2018Review
- The Role of Peripheral CNS-Directed Antibodies in Promoting Inflammatory CNS Demyelination.Brain sciences · 2017Review
- Myelin Oligodendrocyte Glycoprotein: Deciphering a Target in Inflammatory Demyelinating Diseases.Frontiers in immunology · 2017Review
- Microbial Neuraminidase Induces a Moderate and Transient Myelin Vacuolation Independent of Complement System Activation.Frontiers in neurology · 2017Article
- Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model.Nature communications · 2016Article
- Dose-dependent inhibition of demyelination and microglia activation by IVIG.Annals of clinical and translational neurology · 2016Article
- Gut Microbiota Drive Autoimmune Arthritis by Promoting Differentiation and Migration of Peyer's Patch T Follicular Helper Cells.Immunity · 2016Article
- Protection from experimental autoimmune encephalomyelitis by polyclonal IgG requires adjuvant-induced inflammation.Journal of neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The precise mechanisms leading to CNS inflammation and myelin destruction in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) remain the subject of intense debate. In both MS and EAE, autoantibodies (autoAbs) are thought to be involved in tissue destruction through recruiting Fc receptor (FcR)-bearing cells or direct cytotoxic effects through the activation of the complement pathway. Whereas intrathecal immunoglobulin (Ig) production and Ig deposition in inflammatory lesions is a hallmark of MS, mice deficient in B cells and Igs develop severe EAE. Paradoxically, mice of the same genetic background but deficient in FcRgamma are EAE-resistant. We found that the functional expression of FcRgamma on systemic accessory cells, but not CNS-resident cells, appears to be vital for the development of CNS inflammation, independent of antigen-presenting cell function or Ab involvement. On the other hand, we found that the injection of antimyelin oligodendrocyte glycoprotein-Abs drastically worsens disease severity, inflammation, and demyelination. Using FcRgamma(-/-) and C1q(-/-) mice, we could definitively establish that the demyelinating capacity of such autoAb in vivo relies entirely on complement activation and is FcR-independent.
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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.