ArticleJournal of neurology, neurosurgery, and psychiatry2020
Myasthenia gravis AChR antibodies inhibit function of rapsyn-clustered AChRs.
Article in Journal of neurology, neurosurgery, and psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Pathogenic properties of myasthenia gravis AChR autoantibodies associate with clinical response to efgartigimod.Journal of neurology, neurosurgery, and psychiatry · 2026Trial
- Effects of Plasma Exchange Combined with Immunoglobulin Therapy on Consciousness, Immune Function, and Prognosis in Patients with Myasthenia Gravis Crisis: A Prospective Randomized Test.Computational and mathematical methods in medicine · 2022Trial
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Functional Profiling of Acetylcholine Receptor Antibodies Informs Therapeutic Outcome of FcRn Inhibitor Therapy in Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- AChR Autoantibody Pathogenic Properties Are Heterogeneously Distributed and Undergo Temporal Changes Among Patients With Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Article
- AChR-blocking antibodies and complement system dynamics: evaluating their interplay and clinical implications in myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
- Myasthenia gravis: the future is here.The Journal of clinical investigation · 2024Review
- Role of complement in myasthenia gravis.Frontiers in neurology · 2023Review
- Novel pathophysiological insights in autoimmune myasthenia gravis.Current opinion in neurology · 2022Review
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- The Structure, Function, and Physiology of the Fetal and Adult Acetylcholine Receptor in Muscle.Frontiers in molecular neuroscience · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveDirect inhibition of acetylcholine receptor (AChR) function by autoantibodies (Abs) is considered a rare pathogenic mechanism in myasthenia gravis (MG), but is usually studied on AChRs expressed in cell lines, rather than tightly clustered by the intracellular scaffolding protein, rapsyn, as at the intact neuromuscular junction. We hypothesised that clustered AChRs would provide a better target for investigating the functional effects of AChR-Abs.
methodsAcetylcholine-induced currents were measured using whole-cell patch clamping and a fast perfusion system to assess fast (<2 min) functional effects of the serum samples. The sensitivity, specificity and rapidity of the system were first demonstrated by applying maternal AChR-Ab positive plasmas known to inhibit fetal AChR function in TE671 cells. Eleven previously untested AChR-Ab positive MG sera, 10 AChR-Ab negative MG sera and 5 healthy control sera were then applied to unclustered and rapsyn-clustered human adult AChRs in CN21 cells.
resultsThe maternal AChR-Ab positive plasmas reduced fetal AChR currents, but not adult AChR currents, by >80% within 100 s. Only 2/11 AChR-Ab positive sera inhibited AChR currents in unclustered AChRs, but 6/11 AChR-Ab positive sera compared with none of the 10 AChR-Ab negative sera (p=0.0020) inhibited rapsyn-clustered AChR currents, and current inhibition by the AChR-Ab positive sera was greater when the AChRs were clustered (p=0.0385). None of the sera had detectable effects on desensitisation or recovery from desensitisation.
conclusionThese results show that antibodies can inhibit AChR function rapidly and demonstrate the importance of clustering in exploring pathogenic disease mechanisms of MG Abs.
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