ArticleFrontiers in immunology2025
Subtype-specific atypical B cell profiles in myasthenia gravis reveal distinct immunopathological pathways.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association between serum immunoglobulin G4 levels and Graves' ophthalmopathy: a meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Who Can Safely Discontinue Treatment in Myasthenia Gravis? Insights From a Long-Term Real-World Study.European journal of neurology · 2026Article
- The pathogenic role of double-negative B cells in autoimmune diseases.Frontiers in immunology · 2026Review
- The immune microenvironment and population heterogeneity in myasthenia gravis: implications for precision therapeutics.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Atypical B cell (atBC) subsets display significant heterogeneity across autoimmune diseases, complicating efforts to define their role and therapeutic potential. We hypothesized that this heterogeneity reflects the responses to specific immunopathology, resulting in disease-specific profiles. The myasthenia gravis (MG) subtypes acetylcholine receptor (AChR)-positive MG and muscle-specific kinase (MuSK)-positive MG provide an ideal model to explore atBCs due to the distinct immune mechanisms driven by IgG1-3 and IgG4 autoantibodies, respectively in the disease. Methods: CD11c Results: CD11c Discussion: MG subtypes exhibit distinct atBC profiles linked to immunopathology and disease onset. These findings reveal subtype-specific pathways that regulate atBCs and highlight their potential as therapeutic targets in both IgG1-3- and IgG4-mediated autoimmunity.
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Registered trials
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