Observational studyNeurology(R) neuroimmunology & neuroinflammation2023
CD59 Expression in Skeletal Muscles and Its Role in Myasthenia Gravis.
Observational study in Neurology(R) neuroimmunology & neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Complement C3 inhibition restores myasthenia gravis AChR antibody-mediated muscle pathophysiology.EBioMedicine · 2026Article
- Endothelial cell-secreted SPARC suppresses astrocytic CD59 expression and promotes astrocytopathy in a mouse model of neuromyelitis optica spectrum disorders.Nature communications · 2026Article
- Therapeutic strategies targeting complement in myasthenia gravis patients.Journal of neurology · 2025Review
- Ravulizumab for generalized Myasthenia Gravis: a multicenter real-life experience.Journal of neurology · 2025Article
- The role of complement in the immunopathogenesis of acetylcholine receptor antibody-positive generalized myasthenia gravis: bystander or key player?Frontiers in immunology · 2025Review
- Advances in the genetics of myasthenia gravis: insights from cutting-edge neuroscience research.Frontiers in medicine · 2024Review
- Advancements in 2D and 3D In Vitro Models for Studying Neuromuscular Diseases.International journal of molecular sciences · 2023Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesComplement regulatory proteins at the neuromuscular junction (NMJ) could offer protection against complement-mediated damage in myasthenia gravis (MG). However, there is limited information on their expression at the human NMJ. Thus, this study aimed at investigating the expression of the cluster of differentiation 59 (CD59) at the NMJ of human muscle specimens and demonstrating the overexpression of
methodsIn this observational study, muscle specimens from 16 patients with MG (9 and 7 patients with and without thymoma, respectively) and 6 nonmyopathy control patients were examined. Immunohistochemical stains, Western blot analysis, and quantitative real-time reverse transcription PCR were used to evaluate the CD59 expression.
resultsA strong localized expression of CD59 was observed at the NMJ in both patients with and without MG. Moreover, the CD59/glyceraldehyde-3-phosphate dehydrogenase protein ratio in patients with MG was significantly higher than that in the nonmyopathy controls (MG; n = 16, median 0.16, interquartile range (IQR) 0.08-0.26 and nonmyopathy controls; n = 6, median 0.03, IQR 0.02-0.11, DISCUSSION: CD59, which acts as a complement regulator, may protect the NMJ from complement attack. Our findings could provide a basis for further research that investigates the underlying pathogenesis in MG and the immunomodulating interactions of the muscle cells.
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