ArticleNeuroscience2018
Induction of Anti-agrin Antibodies Causes Myasthenia Gravis in Mice.
Article in Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Monoclonal antibody passive experimental autoimmune myasthenia gravis: current progress and future directions.Cell & bioscience · 2026Review
- Clinical utility of human leukocyte antigen genotyping and immunoglobulin G4 autoantibody testing in autoimmune neurological diseases: A focused minireview.World journal of biological chemistry · 2026Review
- Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024Review
- Triple-seronegative myasthenia gravis: clinical and epidemiological characteristics.Arquivos de neuro-psiquiatria · 2024Article
- Pathophysiology of Childhood-Onset Myasthenia: Abnormalities of Neuromuscular Junction and Autoimmunity and Its Background.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Novel pathophysiological insights in autoimmune myasthenia gravis.Current opinion in neurology · 2022Review
- Impaired signaling for neuromuscular synaptic maintenance is a feature of Motor Neuron Disease.Acta neuropathologica communications · 2022Article
- Antibody Therapies in Autoimmune Neuromuscular Junction Disorders: Approach to Myasthenic Crisis and Chronic Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Article
- Antibodies to Full-Length Agrin Protein in Chinese Patients With Myasthenia Gravis.Frontiers in immunology · 2021Article
- Clinical features of LRP4/agrin-antibody-positive myasthenia gravis: A multicenter study.Muscle & nerve · 2020Article
- Myasthenia Gravis: Autoantibody Specificities and Their Role in MG Management.Frontiers in neurology · 2020Review
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- Autoantibody Specificities in Myasthenia Gravis; Implications for Improved Diagnostics and Therapeutics.Frontiers in immunology · 2020Review
- Review
- Review
- The Muscle Is Not a Passive Target in Myasthenia Gravis.Frontiers in neurology · 2019Review
- Understanding the burden of refractory myasthenia gravis.Therapeutic advances in neurological disorders · 2019Review
- Sarcoglycan Alpha Mitigates Neuromuscular Junction Decline in Aged Mice by Stabilizing LRP4.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction (NMJ). Most cases of MG are caused by autoantibodies against the acetylcholine receptor (AChR), muscle-specific kinase (MuSK) and low-density lipoprotein receptor-related protein 4 (LRP4). Recent studies have identified anti-agrin antibodies in MG patients lacking these three antibodies (i.e., triple negative MG). Agrin is a basal lamina protein that has two isoforms. Neural agrin (N-agrin) binds to LRP4 to activate MuSK to induce AChR clusters and is thus critical for NMJ formation. We demonstrate that mice immunized with N-agrin showed MG-associated symptoms including muscle weakness, fragmented and distorted NMJs. These effects were not observed in mice injected with muscle agrin (M-agrin), an isoform that is inactive in inducing AChR clusters. Treatment with anti-N-agrin, but not anti-M-agrin, antibodies reduced agrin-induced AChR clusters in muscle cells. Together, these observations suggest that agrin antibodies may be play a role in MG pathogenesis.
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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.