ArticleBiomedicines2022
Complement Activation Profile in Myasthenia Gravis Patients: Perspectives for Tailoring Anti-Complement Therapy.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Proteomic and machine learning analysis predicts treatment response signatures in Myasthenia Gravis.Journal of translational medicine · 2026Trial
- On the road to blood biomarkers in myasthenia gravis (MG): Beyond clinical scales.Journal of neuromuscular diseases · 2026Review
- Real-world efficacy of eculizumab in generalized myasthenia gravis patients with poor early response to efgartigimod: a prospective cohort study.Frontiers in immunology · 2026Article
- 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
- Refocusing generalized myasthenia gravis: Patient burden, disease profiles, and the role of evolving therapy.European journal of neurology · 2024Review
- Targeting autoimmune mechanisms by precision medicine in Myasthenia Gravis.Frontiers in immunology · 2024Review
- Ravulizumab in Myasthenia Gravis: A Review of the Current Evidence.Neuropsychiatric disease and treatment · 2023Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
The complement system plays a key role in myasthenia gravis (MG). Anti-complement drugs are emerging as effective therapies to treat anti-acetylcholine receptor (AChR) antibody-positive MG patients, though their usage is still limited by the high costs. Here, we searched for plasma complement proteins as indicators of complement activation status in AChR-MG patients, and potential biomarkers for tailoring anti-complement therapy in MG. Plasma was collected from AChR-MG and MuSK-MG patients, and healthy controls. Multiplex immunoassays and ELISA were used to quantify a panel of complement components (C1Q, C2, C3, C4, C5, Factor B, Factor H, MBL, and properdin) and activation products (C4b, C3b, C5a, and C5b-9), of classical, alternative and lectin pathways. C2 and C5 levels were significantly reduced, and C3, C3b, and C5a increased, in plasma of AChR-MG, but not MuSK-MG, patients compared to controls. This protein profile was indicative of complement activation. We obtained sensitivity and specificity performance results suggesting plasma C2, C3, C3b, and C5 as biomarkers for AChR-MG. Our findings reveal a plasma complement "C2, C3, C5, C3b, and C5a" profile associated with AChR-MG to be further investigated as a biomarker of complement activation status in AChR-MG patients, opening new perspectives for tailoring of anti-complement therapies to improve the disease treatment.
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Registered trials
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