ArticleActa neuropathologica communications2017
Myelin-specific multiple sclerosis antibodies cause complement-dependent oligodendrocyte loss and demyelination.
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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
45 citing papers in PubMed, 71 citations in OpenAlex.
- CSF1R inhibition following antibody mediated demyelination has limited impact on remyelination.Acta neuropathologica communications · 2026Article
- Increased VH4+JH6+ antibody heavy chain use in plasmablasts from asymptomatic multiple sclerosis patients.Genes and immunity · 2026Article
- T Helper Cells and Cytokine Networks in the Immunopathogenesis of Multiple Sclerosis.ImmunoTargets and therapy · 2026Review
- SnRNA-seq Interprets Mechanisms by which Three Glial Cell Types Influence Myelin Regeneration in Adult Drug-Resistant Epilepsy-Related Cognitive Impairment.Molecular neurobiology · 2025Article
- Analysis of optic neuritis risk in patients with allergic diseases.Scientific reports · 2025Article
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
- Optic neuritis as a link between autoimmunity and dementia risk.Communications medicine · 2025Article
- Association of optic neuritis with incident depressive disorder risk in a Korean nationwide cohort.Scientific reports · 2025Article
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- BTK regulates microglial function and neuroinflammation in human stem cell models and mouse models of multiple sclerosis.Nature communications · 2024Article
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- OpenSTED: open-source dynamic intensity minimum system for stimulated emission depletion microscopy.Neurophotonics · 2024Article
- Astrocytic stress response is induced by exposure to astrocyte-binding antibodies expressed by plasmablasts from pediatric patients with acute transverse myelitis.Journal of neuroinflammation · 2024Article
- The Plasticity of Immune Cell Response Complicates Dissecting the Underlying Pathology of Multiple Sclerosis.Journal of immunology research · 2024Review
- The pathogenesis of multiple sclerosis: a series of unfortunate events.Clinical and experimental immunology · 2023Article
- Pathogenic myelin-specific antibodies in multiple sclerosis target conformational proteolipid protein 1-anchored membrane domains.The Journal of clinical investigation · 2023Article
- Therapeutic Plasma Exchange and Multiple Sclerosis Dysregulations: Focus on the Removal of Pathogenic Circulatory Factors and Altering Nerve Growth Factor and Sphingosine-1-Phosphate Plasma Levels.Current issues in molecular biology · 2023Review
- Cerebrospinal fluid immunoglobulins in primary progressive multiple sclerosis are pathogenic.Brain : a journal of neurology · 2023Article
- Trisomy 21 induces pericentrosomal crowding delaying primary ciliogenesis and mouse cerebellar development.eLife · 2023Article
- Understanding humoral immunity and multiple sclerosis severity in Black, and Latinx patients.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Intrathecal immunoglobulin G (IgG) synthesis, cerebrospinal fluid (CSF) oligoclonal IgG bands and lesional IgG deposition are seminal features of multiple sclerosis (MS) disease pathology. Both the specific targets and pathogenic effects of MS antibodies remain poorly characterized. We produced IgG1 monoclonal recombinant antibodies (rAbs) from clonally-expanded plasmablasts recovered from MS patient CSF. Among these were a subset of myelin-specific MS rAbs. We examined their immunoreactivity to mouse organotypic cerebellar slices by live binding and evaluated tissue injury in the presence and absence of human complement. Demyelination, glial and neuronal viability, and complement pathway activation were assayed by immunofluorescence microscopy and compared to the effects of an aquaporin-4 water channel (AQP4)-specific rAb derived from a neuromyelitis optica (NMO) patient. MS myelin-specific rAbs bound to discrete surface domains on oligodendrocyte processes and myelinating axons. Myelin-specific MS rAbs initiated complement-dependent cytotoxicity to oligodendrocytes and induced rapid demyelination. Demyelination was accompanied by increased microglia activation; however, the morphology and survival of astrocytes, oligodendrocyte progenitors and neurons remained unaffected. In contrast, NMO AQP4-specific rAb initiated complement-dependent astrocyte damage, followed by sequential loss of oligodendrocytes, demyelination, microglia activation and neuronal death. Myelin-specific MS antibodies cause oligodendrocyte loss and demyelination in organotypic cerebellar slices, which are distinct from AQP4-targeted pathology, and display seminal features of active MS lesions. Myelin-specific antibodies may play an active role in MS lesion formation through complement-dependent mechanisms.
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.