ReviewAnnals of the New York Academy of Sciences2012
The role of complement in experimental autoimmune myasthenia gravis.
Review in Annals of the New York Academy of Sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07215949 (Zilucoplan Treatment of Severe MG Exacerbations Leading to Hospitalization of Participants With Acetylcholine Receptor Antibody Positive gMG), which is not on this map. Cited by 7 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.
Zilucoplan Treatment of Severe MG Exacerbations Leading to Hospitalization of Participants With Acetylcholine Receptor Antibody Positive gMG
Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- Myasthenia gravis: from recognition of heterogeneity to a paradigm shift toward precision therapy.Frontiers in immunology · 2026Review
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Cardiac troponin T and autoimmunity in skeletal muscle aging.GeroScience · 2022Article
- New Approaches to Targeting B Cells for Myasthenia Gravis Therapy.Frontiers in immunology · 2020Review
- IgG1 deficiency exacerbates experimental autoimmune myasthenia gravis in BALB/c mice.Journal of neuroimmunology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Complement plays an important role in the pathophysiology of experimental autoimmune myasthenia gravis (EAMG). The deposition of IgG at the neuromuscular junction, followed by the activation and observance of C3 at the site, and finally the insertion of the membrane attack complex results in the destruction of the plasma membrane at the neuromuscular junction. Animal models of complement-deficient components show the importance of the mediated lysis in EAMG. These events have regulators that allow for the limitation in the cascade and the ability of the cell to inhibit complement at many places along the pathway. The complement regulatory proteins have many roles in reducing the activation of the complement cascade and the inflammatory pathways. Mice deficient in complement regulatory proteins, decay accelerating factor, and CD59 demonstrate a significant increase in the destruction at the neuromuscular junction. Inhibition of complement-mediated lysis is an attractive therapeutic in MG.
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.