ArticleClinical and experimental immunology2006
The membrane attack pathway of complement drives pathology in passively induced experimental autoimmune myasthenia gravis in mice.
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 56 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Rituximab for myasthenia gravis.The Cochrane database of systematic reviews · 2025Pooled it
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- Monoclonal antibody passive experimental autoimmune myasthenia gravis: current progress and future directions.Cell & bioscience · 2026Review
- Complement inhibitors for myasthenia gravis in adults.The Cochrane database of systematic reviews · 2025Article
- Immunomodulators and immunosuppressants for myasthenia gravis: a network meta-analysis.The Cochrane database of systematic reviews · 2025Article
- Systemic lupus erythematosus as the paradigm for understanding the complex immune relationships and therapeutic opportunities for targeting complement in autoimmune diseases.Immunobiology · 2025Review
- The role of complement in the immunopathogenesis of acetylcholine receptor antibody-positive generalized myasthenia gravis: bystander or key player?Frontiers in immunology · 2025Review
- Treating myasthenia gravis beyond the eye clinic.Eye (London, England) · 2024Review
- Extreme Tolerance of Extraocular Muscles to Diseases and Aging: Why and How?International journal of molecular sciences · 2024Review
- Article
- Roles of FcRn in Antigen-Presenting Cells during Autoimmunity and a Clinical Evaluation of Efgartigimod as an FcRn Blocker.Pathogens (Basel, Switzerland) · 2023Review
- Identification of potent siRNA targeting complement C5 and its robust activity in pre-clinical models of myasthenia gravis and collagen-induced arthritis.Molecular therapy. Nucleic acids · 2023Article
- Impact of Ravulizumab on Patient Outcomes and Quality of Life in Generalized Myasthenia Gravis.Patient related outcome measures · 2023Review
- FcRN receptor antagonists in the management of myasthenia gravis.Frontiers in neurology · 2023Review
- Terminal complement pathway activation drives synaptic loss in Alzheimer's disease models.Acta neuropathologica communications · 2022Article
- Myasthenia gravis in clinical practice.Arquivos de neuro-psiquiatria · 2022Review
- Divergent complement system activation in two clinically distinct murine models of multiple sclerosis.Frontiers in immunology · 2022Article
- The emerging role of complement in neuromuscular disorders.Seminars in immunopathology · 2021Review
- The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021Review
- Myasthenia Gravis: Epidemiology, Pathophysiology and Clinical Manifestations.Journal of clinical medicine · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The human neuromuscular disease myasthenia gravis (MG) is characterized by the generation of autoantibodies reactive with nicotinic acetylcholine receptors (AChR) that cause loss of AChR from the neuromuscular end-plate with resultant failure of neuromuscular transmission. A role for complement (C) in AChR loss has been suggested based upon morphological identification of C at the end-plate in MG and from the effects of C inhibition in murine models. Here we provide further evidence implicating C, and specifically the membrane attack complex (MAC), in a mouse model of MG. Mice deficient in the C regulators Daf1 and/or Cd59a were tested in the model. Wild-type mice were resistant to disease while mice deficient in Daf1 had mild disease symptoms with evidence of C activation and AChR loss at end-plates. Cd59a-deficient mice had very mild disease with some muscle inflammation and essentially undamaged end-plates. In contrast, mice deficient in both C regulators developed a severe paralytic disease with marked muscle inflammation and loss of end-plates. Inhibition of MAC assembly abrogated clinical disease in these double-deficient mice, demonstrating conclusively that MAC formation was driving pathology in the model. These findings provoke us to suggest that current anti-C therapeutics targeting MAC assembly will be beneficial in MG patients resistant to conventional therapies.
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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.