ArticleScientific reports2018
Human IgM antibody rHIgM22 promotes phagocytic clearance of myelin debris by microglia.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- The Cell-Specific Effects of the Human Remyelination-Promoting rHIgM22 on Sphingolipid Metabolism in Cultured Glial Cells.Neurochemical research · 2026Article
- How do different cell populations orchestrate myelin regeneration?Biochemical Society transactions · 2025Review
- Phospholipase D Family Member 4 Regulates Microglial Phagocytosis and Remyelination via the AKT Pathway in a Cuprizone-Induced Multiple Sclerosis Mouse Model.CNS neuroscience & therapeutics · 2024Article
- The interplay of inflammation and remyelination: rethinking MS treatment with a focus on oligodendrocyte progenitor cells.Molecular neurodegeneration · 2024Review
- Identification of the Lipid Antigens Recognized by rHIgM22, a Remyelination-Promoting Antibody.Neurochemical research · 2023Article
- The roles of microglia and astrocytes in myelin phagocytosis in the central nervous system.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Immune response of BV-2 microglial cells is impacted by peroxisomal beta-oxidation.Frontiers in molecular neuroscience · 2023Article
- Optic Neuritis in Multiple Sclerosis-A Review of Molecular Mechanisms Involved in the Degenerative Process.Current issues in molecular biology · 2022Review
- Breaking the barriers to remyelination in multiple sclerosis.Current opinion in pharmacology · 2022Review
- The Forgotten Brother: The Innate-like B1 Cell in Multiple Sclerosis.Biomedicines · 2022Review
- Autoreactive antibodies control blood glucose by regulating insulin homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Rheumatoid factor IgM autoantibodies control IgG homeostasis.Frontiers in immunology · 2022Article
- Tissues: the unexplored frontier of antibody mediated immunity.Current opinion in virology · 2021Review
- The Role of Distinct Subsets of Macrophages in the Pathogenesis of MS and the Impact of Different Therapeutic Agents on These Populations.Frontiers in immunology · 2021Review
- Myelin Repair: From Animal Models to Humans.Frontiers in cellular neuroscience · 2021Review
- Remyelination-Promoting DNA Aptamer Conjugate Myaptavin-3064 Binds to Adult Oligodendrocytes In Vitro.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Microglial Phagocytosis-Rational but Challenging Therapeutic Target in Multiple Sclerosis.International journal of molecular sciences · 2020Review
- Astrocytes and Microglia as Major Players of Myelin Production in Normal and Pathological Conditions.Frontiers in cellular neuroscience · 2020Review
- Activated human astrocyte-derived extracellular vesicles modulate neuronal uptake, differentiation and firing.Journal of extracellular vesicles · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
In multiple sclerosis (MS), demyelinated CNS lesions fail to sufficiently remyelinate, despite the presence of oligodendrocyte precursor cells (OPCs) capable of differentiating into mature oligodendrocytes. MS lesions contain damaged myelin debris that can inhibit OPC maturation and hinder repair. rHIgM22 is an experimental human recombinant IgM antibody that promotes remyelination in animal models and is being examined in patients with MS. rHIgM22 binds to CNS myelin and partially rescues OPC process outgrowth on myelin. Since rHIgM22 does not affect OPC process outgrowth in vitro on permissive substrate, we examined the possibility that it acts by enhancing phagocytic clearance of myelin debris by microglia. In this study, we tested if rHIgM22 binding could tag myelin for microglial phagocytosis. A mouse microglial cell line and primary rat microglia were treated with myelin and rHIgM22 and assayed for myelin phagocytosis. We found that: 1) rHIgM22 stimulates myelin phagocytosis in a dose-dependent manner; 2) rHIgM22-mediated myelin phagocytosis requires actin polymerization; and 3) rHIgM22-stimulation of myelin phagocytosis requires activity of rHIgM22 Fc domain and activation of Complement Receptor 3. Since myelin inhibits OPC differentiation, stimulation of phagocytic clearance of damaged myelin may be an important means by which rHIgM22 promotes remyelination.
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Registered trials
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