ArticleExpert review of clinical immunology2008
Effect of complement and its regulation on myasthenia gravis pathogenesis.
Article in Expert review of clinical immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed.
- Proteomic and machine learning analysis predicts treatment response signatures in Myasthenia Gravis.Journal of translational medicine · 2026Trial
- Regimen-stratified Bayesian model-based meta-analysis of targeted biologics in generalised myasthenia gravis: efficacy comparison, mechanism-level class contrast, and endpoint sensitivity with model-informed trial design.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Early versus late add-on therapy in generalized myasthenia gravis: a multicenter real-world cohort study.Journal of neurology · 2026Observational
- Proteomic and Machine Learning Analysis Predicts Treatment Response Signatures in Myasthenia Gravis.Research square · 2025Article
- Review
- AChR-blocking antibodies and complement system dynamics: evaluating their interplay and clinical implications in myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- C5 complement inhibition versus FcRn modulation in generalised myasthenia gravis.Journal of neurology, neurosurgery, and psychiatry · 2025Observational
- New and Emerging Biological Therapies for Myasthenia Gravis: A Focussed Review for Clinical Decision-Making.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Review
- Zilucoplan, a macrocyclic peptide inhibitor of human complement component 5, uses a dual mode of action to prevent terminal complement pathway activation.Frontiers in immunology · 2023Article
- CD59 Expression in Skeletal Muscles and Its Role in Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2023Observational
- Eculizumab versus rituximab in generalised myasthenia gravis.Journal of neurology, neurosurgery, and psychiatry · 2022Observational
- In vitro models of neuromuscular junctions and their potential for novel drug discovery and development.Expert opinion on drug discovery · 2020Review
- C3, C5a and anti-acetylcholine receptor antibody as severity biomarkers in myasthenia gravis.Therapeutic advances in neurological disorders · 2020Article
- Retrospective Analysis of Eculizumab in Patients with Acetylcholine Receptor Antibody-Negative Myasthenia Gravis: A Case Series.Journal of neuromuscular diseases · 2020Article
- Viral-derived complement inhibitors: current status and potential role in immunomodulation.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Applying complement therapeutics to rare diseases.Clinical immunology (Orlando, Fla.) · 2015Review
- Targeting therapy to the neuromuscular junction: proof of concept.Muscle & nerve · 2014Article
- Cell surface complement regulators moderate experimental myasthenia gravis pathology.Muscle & nerve · 2013Article
- Biomarker development for 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.
Funding
Abstract
Myasthenia gravis (MG) is primarily caused by antibodies directed towards the skeletal muscle acetylcholine receptor, leading to muscle weakness. Although these antibodies may induce compromise of neuromuscular transmission by blocking acetylcholine receptor function or antigenic modulation, the predominant mechanism of injury to the neuromuscular junction is complement-mediated lysis of the postsynaptic membrane. The vast majority of data to support the role of complement derives from experimentally acquired MG (EAMG). In this article, we review studies that demonstrate the central role of complement in EAMG and MG pathogenesis along with the emerging role of complement in T- and B-cell function, as well as the potential for complement inhibitor-based therapy to treat human MG.
Identifiers
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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.