ArticleMuscle & nerve2013
Cell surface complement regulators moderate experimental myasthenia gravis pathology.
Article in Muscle & nerve, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Mitochondrial dysfunction in myasthenia gravis: Exploring directions for future immunotherapy? A review.Biomolecules & biomedicine · 2025Review
- The role of complement in the immunopathogenesis of acetylcholine receptor antibody-positive generalized myasthenia gravis: bystander or key player?Frontiers in immunology · 2025Review
- Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review.Journal of neurology · 2021Review
- Complementopathies and precision medicine.The Journal of clinical investigation · 2020Review
- Complement Inhibitor Therapy for Myasthenia Gravis.Frontiers in immunology · 2020Review
- Investigational RNAi Therapeutic Targeting C5 Is Efficacious in Pre-clinical Models of Myasthenia Gravis.Molecular therapy. Methods & clinical development · 2019Article
- Pathogenesis of myasthenia gravis: update on disease types, models, and mechanisms.F1000Research · 2016Review
- Applying complement therapeutics to rare diseases.Clinical immunology (Orlando, Fla.) · 2015Review
- Guidelines for pre-clinical assessment of the acetylcholine receptor--specific passive transfer myasthenia gravis model-Recommendations for methods and experimental designs.Experimental neurology · 2015Article
- Targeting therapy to the neuromuscular junction: proof of concept.Muscle & nerve · 2014Article
- Survivin as a potential mediator to support autoreactive cell survival in myasthenia gravis: a human and animal model study.PloS one · 2014Article
- The role of complement in experimental autoimmune myasthenia gravis.Annals of the New York Academy of Sciences · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
introductionIntrinsic mouse complement regulators influence the severity of passively induced experimental acquired myasthenia gravis (EAMG). To assess the potential influence of CD59b in the absence of CD59a background, we used the mCD59ab(-/-) mouse model to re-evaluate mCD59 in protecting the neuromuscular junction (NMJ).
methodsEAMG was induced with monoclonal antibody to the acetylcholine receptor (AChR) in Daf1(-/-) , CD59ab(-/-) , Daf1(-/-) CD59ab(-/-) , and wild-type C57Bl/6 mice. Animals were monitored throughout the experiment. Diaphragms were analyzed for NMJ injury.
resultsDaf1(-/-) CD59ab(-/-) mice required euthanasia 24 hours after disease induction because of severe weakness. Histological assessment demonstrated reduced AChR density, simplification of synaptic folds, and disrupted mitochondria. CD59ab-deficient mice demonstrated mild weakness and reduction in weight after 24 hours. In contrast, Daf1(-/-) had more severe weakness at 60 hours. The NMJ of EAMG-induced Daf1(-/-) and CD59ab(-/-) mice demonstrated similar AChR density.
conclusionNMJs of CD59 and DAF mice are protected from complement-mediated injury of passive EAMG.
Indexed as
Identifiers
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.