ArticleFrontiers in immunology2022
A Targeted Complement Inhibitor CRIg/FH Protects Against Experimental Autoimmune Myasthenia Gravis in Rats
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Anti-C2-mediated complement inhibition prevents disease in a rat passive transfer model of myasthenia gravis.Journal of translational autoimmunity · 2026Article
- Monoclonal antibody passive experimental autoimmune myasthenia gravis: current progress and future directions.Cell & bioscience · 2026Review
- Refinement of the rat acetylcholine receptor-specific passive transfer myasthenia gravis model using subcutaneous injections: an update to the guidelines.Scientific reports · 2025Article
- Therapeutic strategies targeting complement in myasthenia gravis patients.Journal of neurology · 2025Review
- Optimization of Induction Protocols for Experimental Autoimmune Myasthenia Gravis.International journal of molecular sciences · 2025Article
- CG001, a C3b-targeted complement inhibitor, blocks 3 complement pathways: development and preclinical evaluation.Blood advances · 2024Article
- An angel or a devil? Current view on the role of CD8Journal of translational medicine · 2024Review
- Study on the Potential Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- A multi-dimensional phenotyping framework reveals coordinated neuromuscular, immune, and imaging-derived phenotypes in experimental autoimmune myasthenia gravis.Frontiers in neurologyArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibody-induced complement activation may cause injury of the neuromuscular junction (NMJ) and is thus considered as a primary pathogenic factor in human myasthenia gravis (MG) and animal models of experimental autoimmune myasthenia gravis (EAMG). In this study, we tested whether CRIg/FH, a targeted complement inhibitor, could attenuate NMJ injury in rat MG models. We first demonstrated that CRIg/FH could inhibit complement-dependent cytotoxicity on human rhabdomyosarcoma TE671 cells induced by MG patient-derived IgG
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