ArticlePloS one2014
Direct proof of the in vivo pathogenic role of the AChR autoantibodies from myasthenia gravis patients.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Bispecific chimeric autoantibody receptor T cells eliminate acetylcholine receptor-specific B cells in myasthenia gravis models.Nature communications · 2026Article
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Selective Depletion of Autoreactive Plasma Cells as a Novel Strategy to Treat Acetylcholine Receptor Antibody-Positive Myasthenia Gravis.European journal of immunology · 2026Article
- Engineered Bi-Specific AChR CAAR T Cells for Selective Elimination of Myasthenia Gravis B Cells.Research square · 2026Article
- Application analysis of transfected cell method for detecting AChR antibodies in MG patients.Scientific reports · 2026Article
- Subunit-Specific Immunodominance in Clinically Distinct Populations With AChR+ Myasthenia Gravis: A Multiparametric Cross-Sectional Analysis.Neurology · 2025Article
- Hock immunization, a refined alternative for developing experimental autoimmune myasthenia gravis (EAMG) in mice.Scientific reports · 2025Article
- Mitochondrial dysfunction in myasthenia gravis: Exploring directions for future immunotherapy? A review.Biomolecules & biomedicine · 2025Review
- Defective autophagy and autophagy activators in myasthenia gravis: a rare entity and unusual scenario.Autophagy · 2024Review
- Review
- Serological diagnosis of myasthenia gravis and its clinical significance.Annals of translational medicine · 2023Review
- Receptor clustering and pathogenic complement activation in myasthenia gravis depend on synergy between antibodies with multiple subunit specificities.Acta neuropathologica · 2022Article
- Analysis of nAChR Autoantibodies Against Extracellular Epitopes in MG Patients.Frontiers in neurology · 2022Article
- A Recombinant Acetylcholine Receptor α1 Subunit Extracellular Domain Is a Promising New Drug Candidate for Treatment Of Myasthenia Gravis.Frontiers in immunology · 2022Article
- The mitochondrial biogenesis signaling pathway is a potential therapeutic target for myasthenia gravis via energy metabolism (Review).Experimental and therapeutic medicine · 2021Review
- No correlation between acetylcholine receptor antibody concentration and individual clinical symptoms of myasthenia gravis: A systematic retrospective study involving 67 patients.Brain and behavior · 2021Article
- Fc-Receptor Targeted Therapies for the Treatment ofInternational journal of molecular sciences · 2021Review
- Myasthenia Gravis: Epidemiology, Pathophysiology and Clinical Manifestations.Journal of clinical medicine · 2021Review
- Myasthenia Gravis: Autoantibody Specificities and Their Role in MG Management.Frontiers in neurology · 2020Review
- Autoantibody Specificities in Myasthenia Gravis; Implications for Improved Diagnostics and Therapeutics.Frontiers in immunology · 2020Review
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have suggested that the autoantibodies (autoAbs) against muscle acetylcholine receptor (AChR) of myasthenia gravis (MG) patients are the main pathogenic factor in MG; however, this belief has not yet been confirmed with direct observations. Although animals immunized with AChR or injected with anti-AChR monoclonal Abs, or with crude human MG Ig fractions exhibit MG symptoms, the pathogenic role of isolated anti-AChR autoAbs, and, more importantly, the absence of pathogenic factor(s) in the autoAb-depleted MG sera has not yet been shown by in vivo studies. Using recombinant extracellular domains of the human AChR α and β subunits, we have isolated autoAbs from the sera of four MG patients. The ability of these isolated anti-subunit Abs and of the Ab-depleted sera to passively transfer experimental autoimmune MG in Lewis rats was investigated. We found that the isolated anti-subunit Abs were at least as efficient as the corresponding whole sera or whole Ig in causing experimental MG. Abs to both α- and β-subunit were pathogenic although the anti-α-subunit were much more efficient than the anti-β-subunit ones. Interestingly, the autoAb-depleted sera were free of pathogenic activity. The later suggests that the myasthenogenic potency of the studied anti-AChR MG sera is totally due to their anti-AChR autoAbs, and therefore selective elimination of the anti-AChR autoAbs from MG patients may be an efficient therapy for MG.
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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.