ArticleActa neuropathologica communications2015
IL-6 and Akt are involved in muscular pathogenesis in myasthenia gravis.
Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 104 citations in OpenAlex.
- Fatigue in Myasthenia Gravis: Recent Advances and Emerging Concepts.Muscle & nerve · 2026Review
- Integrated Transcriptomic and Machine Learning Analysis Reveals Immune-Related Regulatory Networks in Anti-NMDAR Encephalitis.International journal of molecular sciences · 2026Article
- Interconnection between myasthenia gravis and type 2 diabetes: emerging role of metformin in modulating PI3K/AKT/mTOR/AMPK axis.Metabolic brain disease · 2025Review
- Correlation of C-Reactive Protein With Severe Fatigue in Patients With Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Tocilizumab for the management of corticosteroid-resistant GO combined with OMG: a case series.BMC ophthalmology · 2024Article
- Dramatic improvement in refractory myasthenia gravis with eculizumab treatment: a case report.Journal of neurology · 2024Article
- Responsiveness to Tocilizumab in Anti-Acetylcholine Receptor-Positive Generalized Myasthenia Gravis.Aging and disease · 2024Article
- Dexamethasone improves thymoma-associated myasthenia gravis via the AKT-mTOR pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Article
- Plasma Myokine Profiles in Patients With AChR- and MuSK-Ab-Positive Myasthenia Gravis.Journal of clinical neurology (Seoul, Korea) · 2023Article
- Nomogram for the acute exacerbation of acetylcholine receptor antibody-positive generalized myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Investigation of the Underlying Mechanism of Huangqi-Dangshen for Myasthenia Gravis Treatment via Molecular Docking and Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Expression of TRAF6 in peripheral blood B cells of patients with myasthenia gravis.BMC neurology · 2022Article
- Study on the Potential Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Exploring the Potential Mechanism of Qi-Shen-Di-Huang Drug Formulary for Myasthenia Gravis (MG) based on UHPLC-QE-MS Network Pharmacology and Molecular Docking Techniques.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Histone Deacetylase Isoforms Differentially Modulate Inflammatory and Autoantibody Responses in a Mouse Model of Myasthenia Gravis.Frontiers in neurology · 2021Article
- Gene expression profiling of orbital muscles in treatment-resistant ophthalmoplegic myasthenia gravis.Orphanet journal of rare diseases · 2020Article
- Article
- AChR antibodies show a complex interaction with human skeletal muscle cells in a transcriptomic study.Scientific reports · 2020Article
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Authors and funding
13 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAnti-acetylcholine receptor (AChR) autoantibodies target muscles in spontaneous human myasthenia gravis (MG) and its induced experimental autoimmune model MG (EAMG). The aim of this study was to identify novel functional mechanisms occurring in the muscle pathology of myasthenia.
resultsA transcriptome analysis performed on muscle tissue from MG patients (compared with healthy controls) and from EAMG rats (compared with control rats) revealed a deregulation of genes associated with the Interleukin-6 (IL-6) and Insulin-Like Growth Factor 1 (IGF-1) pathways in both humans and rats. The expression of IL-6 and its receptor IL-6R transcripts was found to be altered in muscles of EAMG rats and mice compared with control animals. In muscle biopsies from MG patients, IL-6 protein level was higher than in control muscles. Using cultures of human muscle cells, we evaluated the effects of anti-AChR antibodies on IL-6 production and on the phosphorylation of Protein Kinase B (PKB/Akt). Most MG sera and some monoclonal anti-AChR antibodies induced a significant increase in IL-6 production by human muscle cells. Furthermore, Akt phosphorylation in response to insulin was decreased in the presence of monoclonal anti-AChR antibodies.
conclusionsAnti-AChR antibodies alter IL-6 production by muscle cells, suggesting a putative novel functional mechanism of action for the anti-AChR antibodies. IL-6 is a myokine with known effects on signaling pathways such as Akt/mTOR (mammalian Target of Rapamycin). Since Akt plays a key role in multiple cellular processes, the reduced phosphorylation of Akt by the anti-AChR antibodies may have a significant impact on the muscle fatigability observed in MG patients.
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