ArticleJCI insight2019
Characterization of pathogenic monoclonal autoantibodies derived from muscle-specific kinase myasthenia gravis patients.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- IgG Subclass (IgG1-4) and IgA Autoantibody Profiles Against Muscle-Specific Kinase in a Greek Cohort.Muscle & nerve · 2026Article
- Muscle-Specific Kinase Signaling and Its Therapeutic Potential.Muscle & nerve · 2026Review
- 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
- MuSK myasthenia gravis: from antigen-antibody to clinical translation.Frontiers in immunology · 2026Review
- Patient-Derived Monoclonal Myelin Oligodendrocyte Glycoprotein Autoantibodies Mediate Cytotoxicity.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- MuSK cysteine-rich domain antibodies are pathogenic in a mouse model of autoimmune myasthenia gravis.The Journal of clinical investigation · 2025Article
- Myasthenia gravis in 2025: five new things and four hopes for the future.Journal of neurology · 2025Review
- A pilot study of the immunological profile and efficacy of rituximab in muscle-specific kinase antibody-positive myasthenia gravis.Frontiers in immunology · 2025Article
- Antibodies in neurological diseases: Established, emerging, explorative.Immunological reviews · 2024Review
- Decoding myasthenia gravis: advanced diagnosis with infrared spectroscopy and machine learning.Scientific reports · 2024Article
- Gut microbiota-derived butyrate restores impaired regulatory T cells in patients with AChR myasthenia gravis via mTOR-mediated autophagy.Cell communication and signaling : CCS · 2024Article
- Exploring the depths of IgG4: insights into autoimmunity and novel treatments.Frontiers in immunology · 2024Review
- A clinical perspective on muscle specific kinase antibody positive myasthenia gravis.Frontiers in immunology · 2024Review
- Advances in B Cell Targeting for Treating Muscle-Specific Tyrosine Kinase-Associated Myasthenia Gravis.ImmunoTargets and therapy · 2024Review
- IgG1-3 MuSK Antibodies Inhibit AChR Cluster Formation, Restored by SHP2 Inhibitor, Despite Normal MuSK, DOK7, or AChR Subunit Phosphorylation.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Precision targeting of autoantigen-specific B cells in muscle-specific tyrosine kinase myasthenia gravis with chimeric autoantibody receptor T cells.Nature biotechnology · 2023Article
- Individual myasthenia gravis autoantibody clones can efficiently mediate multiple mechanisms of pathology.Acta neuropathologica · 2023Article
- Clinicoserological insights into patients with immune checkpoint inhibitor-induced myasthenia gravis.Annals of clinical and translational neurology · 2023Article
- Validation of Ligand Tetramers for the Detection of Antigen-Specific Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by muscle weakness and caused by pathogenic autoantibodies that bind to membrane proteins at the neuromuscular junction. Most patients have autoantibodies against the acetylcholine receptor (AChR), but a subset of patients have autoantibodies against muscle-specific tyrosine kinase (MuSK) instead. MuSK is an essential component of the pathway responsible for synaptic differentiation, which is activated by nerve-released agrin. Through binding MuSK, serum-derived autoantibodies inhibit agrin-induced MuSK autophosphorylation, impair clustering of AChRs, and block neuromuscular transmission. We sought to establish individual MuSK autoantibody clones so that the autoimmune mechanisms could be better understood. We isolated MuSK autoantibody-expressing B cells from 6 MuSK MG patients using a fluorescently tagged MuSK antigen multimer, then generated a panel of human monoclonal autoantibodies (mAbs) from these cells. Here we focused on 3 highly specific mAbs that bound quantitatively to MuSK in solution, to MuSK-expressing HEK cells, and at mouse neuromuscular junctions, where they colocalized with AChRs. These 3 IgG isotype mAbs (2 IgG4 and 1 IgG3 subclass) recognized the Ig-like domain 2 of MuSK. The mAbs inhibited AChR clustering, but intriguingly, they enhanced rather than inhibited MuSK phosphorylation, which suggests an alternative mechanism for inhibiting AChR clustering.
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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.