ArticleActa neuropathologica2022
Receptor clustering and pathogenic complement activation in myasthenia gravis depend on synergy between antibodies with multiple subunit specificities.
Article in Acta neuropathologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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
37 citing papers in PubMed, 45 citations in OpenAlex.
- Pathogenic properties of myasthenia gravis AChR autoantibodies associate with clinical response to efgartigimod.Journal of neurology, neurosurgery, and psychiatry · 2026Trial
- Time to response with ravulizumab, a long-acting terminal complement inhibitor, in adults with anti-acetylcholine receptor antibody-positive generalized myasthenia gravis.European journal of neurology · 2024Trial
- Long-term efficacy and safety of ravulizumab in adults with anti-acetylcholine receptor antibody-positive generalized myasthenia gravis: results from the phase 3 CHAMPION MG open-label extension.Journal of neurology · 2023Trial
- Ravulizumab pharmacokinetics and pharmacodynamics in patients with generalized myasthenia gravis.Journal of neurology · 2023Trial
- Longitudinal dynamics and clinical significance of acetylcholine receptor blocking antibodies in myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Bispecific chimeric autoantibody receptor T cells eliminate acetylcholine receptor-specific B cells in myasthenia gravis models.Nature communications · 2026Article
- Functional Profiling of Acetylcholine Receptor Antibodies Informs Therapeutic Outcome of FcRn Inhibitor Therapy in Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- IgA autoantibodies demonstrate a novel mechanism of MuSK myasthenia gravis pathology.Brain : a journal of neurology · 2026Article
- Monoclonal antibody passive experimental autoimmune myasthenia gravis: current progress and future directions.Cell & bioscience · 2026Review
- Generation of Monoclonal Autoantibodies From Myelin Oligodendrocyte Glycoprotein-Specific Human B Cells Using an Optofluidic-Based Platform.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Engineered Bi-Specific AChR CAAR T Cells for Selective Elimination of Myasthenia Gravis B Cells.Research square · 2026Article
- Patient-Derived Monoclonal Myelin Oligodendrocyte Glycoprotein Autoantibodies Mediate Cytotoxicity.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Seropositive Myasthenia Gravis Triggered by Lyme Disease: A Case Study of Molecular Mimicry.Cureus · 2025Article
- Therapeutic IgG- and IgM-specific proteases disarm the acetylcholine receptor autoantibodies that drive myasthenia gravis pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- AChR Autoantibody Pathogenic Properties Are Heterogeneously Distributed and Undergo Temporal Changes Among Patients With Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Review
- Article
- Composition and function of AChR chimeric autoantibody receptor T cells for antigen-specific B cell depletion in myasthenia gravis.Science advances · 2025Article
- Myasthenia gravis in 2025: five new things and four hopes for the future.Journal of neurology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myasthenia gravis is an autoimmune disorder defined by muscle weakness and fatigability associated with antibodies against proteins of the neuromuscular junction (NMJ). The most common autoantibody target is the acetylcholine receptor (AChR). Three mechanisms have been postulated by which autoantibodies might interfere with neurotransmission: direct antagonism of the receptor, complement-mediated destruction of the postsynaptic membrane, and enhanced internalization of the receptor. It is very likely that more than one of these mechanisms act in parallel. Dissecting the mechanisms of autoantibody-mediated pathology requires patient-derived, monoclonal antibodies. Using membrane antigen capture activated cell sorting (MACACS), we isolated AChR-specific B cells from patients with myasthenia gravis, and produced six recombinant antibodies. All AChR-specific antibodies were hypermutated, including isotypes IgG
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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.