ArticleClinical and experimental immunology2006
Complement membrane attack is required for endplate damage and clinical disease in passive experimental myasthenia gravis in Lewis rats.
Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 66 citations in OpenAlex.
- Early versus late add-on therapy in generalized myasthenia gravis: a multicenter real-world cohort study.Journal of neurology · 2026Observational
- FcRn antagonist and C5 complement inhibitor as early rescue strategies in severe Myasthenia Gravis: a two-case report.Frontiers in immunology · 2026Article
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- Review
- 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
- The role of complement in the immunopathogenesis of acetylcholine receptor antibody-positive generalized myasthenia gravis: bystander or key player?Frontiers in immunology · 2025Review
- Consensus guidelines on the diagnosis and management of myasthenia gravis by the Saudi Arabia Neuromuscular and Electrodiagnostic Medicine and neuromuscular specialists from the Gulf Cooperation Council region.Therapeutic advances in neurological disorders · 2025Review
- Myasthenia gravis: the changing treatment landscape in the era of molecular therapies.Nature reviews. Neurology · 2024Review
- Role of complement in myasthenia gravis.Frontiers in neurology · 2023Review
- Cardiac troponin T and autoimmunity in skeletal muscle aging.GeroScience · 2022Article
- Terminal complement pathway activation drives synaptic loss in Alzheimer's disease models.Acta neuropathologica communications · 2022Article
- Discovery of functionally distinct anti-C7 monoclonal antibodies and stratification of anti-nicotinic AChR positive Myasthenia Gravis patients.Frontiers in immunology · 2022Article
- The emerging role of complement in neuromuscular disorders.Seminars in immunopathology · 2021Review
- Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review.Journal of neurology · 2021Review
- Complement in neurological disorders and emerging complement-targeted therapeutics.Nature reviews. Neurology · 2020Review
- Complementopathies and precision medicine.The Journal of clinical investigation · 2020Review
- Complement Inhibitor Therapy for Myasthenia Gravis.Frontiers in immunology · 2020Review
- Complement Inhibition for the Treatment of Myasthenia Gravis.ImmunoTargets and therapy · 2020Review
- Monoclonal Antibodies Capable of Inhibiting Complement Downstream of C5 in Multiple Species.Frontiers in immunology · 2020Article
- C3, C5a and anti-acetylcholine receptor antibody as severity biomarkers in myasthenia gravis.Therapeutic advances in neurological disorders · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Myasthenia gravis (MG) is a debilitating and potentially fatal neuromuscular disease characterized by the generation of autoantibodies reactive with nicotinic acetylcholine receptors (AChR) that cause loss of AChR from the neuromuscular endplate with resultant failure of neuromuscular transmission. A role for complement (C) in the pathology of human MG has been suggested based upon identification of C activation products in plasma and deposited at the endplate in MG. In the rat model, experimental autoimmune MG (EAMG), C depletion or inhibition restricts clinical disease, further implicating C in pathology. The mechanisms by which C activation drives pathology in MG and EAMG are unclear. Here we provide further evidence implicating C and specifically the membrane attack complex (MAC) in the Lewis rat passive EAMG model of MG. Rats deficient in C6, an essential component of the MAC, were resistant to disease induction and endplate destruction was reduced markedly compared to C6-sufficient controls. After reconstitution with C6, disease severity and endplate destruction in the C6-deficient rats was equivalent to that in controls. The data confirm the essential role of the MAC in the destruction of the endplate in EAMG and raise the prospect of specific MAC inhibition as an alternative therapy in MG patients resistant to conventional treatments.
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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.