ArticleClinical and translational medicine2025
Single-cell atlas reveals heterogeneous response to FcRn blockade in anti-AChR antibody-positive generalised myasthenia gravis.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Efgartigimod Versus Lymphoplasmapheresis as Preoperative Rapid Antibody-Clearing Therapies for Thymectomy in Generalized Myasthenia Gravis: Effectiveness, Safety and Cost Outcomes Compared to Conventional Preparation.CNS neuroscience & therapeutics · 2026Article
- B Cells and B Cell Depletion in Autoimmunity and Atherosclerosis.Life (Basel, Switzerland) · 2026Review
- In-Depth Profiling Highlights the Effect of Efgartigimod on Peripheral Innate and Adaptive Immune Cells in Myasthenia Gravis.Annals of clinical and translational neurology · 2026Article
- Current status and challenges of biologic targeted therapy for myasthenia gravis in China.Intractable & rare diseases research · 2026Review
- Long-term use of rozanolixizumab in generalised myasthenia gravis: final pooled analysis of the phase III MycarinG study and two open-label extensions.Therapeutic advances in neurological disorders · 2026Article
- The immune microenvironment and population heterogeneity in myasthenia gravis: implications for precision therapeutics.Frontiers in immunology · 2026Review
- Single-cell atlas reveals heterogeneous response to FcRn blockade in anti-AChR antibody-positive generalised myasthenia gravis.Clinical and translational medicine · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundMyasthenia gravis (MG) is an autoimmune disease predominantly driven by autoantibodies targeting acetylcholine receptor (AChR), resulting in muscle weakness. Efgartigimod, a neonatal Fc receptor (FcRn) blocker, reduces pathogenic immunoglobulin G in anti-AChR antibody-positive generalised MG (gMG). This study aimed to identify immune mechanisms underlying MG pathology and response to efgartigimod.
methodsWe constructed a single-cell atlas of peripheral immune cells from treatment-naïve and efgartigimod-treated patients with gMG. Comprehensive immunophenotyping was performed to compare the clonal diversity of B- and T-cell populations, alongside experimental validation to assess the activation of Th17-related pathways before and after FcRn blockade.
resultsB cells in patients with gMG exhibit heightened activation and differentiation, while T cells display distinct pro-inflammatory phenotypes. Enhanced intercellular signalling contributed to the pathogenicity associated with gMG. Efgartigimod mitigated upregulated antigen processing and presentation pathways in MG. Additionally, B-cell clonal diversity and IGHG1-bearing B-cell receptors increased. Transcriptional factor alterations were noted in suboptimal responders. Regulation of T-cell activity, particularly within Th17-related pathways, was associated with remission rates.
conclusionsThese findings underscore immune heterogeneity and dynamics during efgartigimod treatment, providing mechanistic insights into therapeutic response in gMG. KEY POINTS: Aberrant B cells and pro-inflammatory T cells contribute critically to generalised myasthenia gravis (gMG) pathogenesis. Neonatal Fc receptor (FcRn) blockade induces immunoglobulin G (IgG) depletion feedback, reflected by increased class-switched BCRs. Th17 cell proliferation is attenuated following FcRn blockade. Antigen processing and presentation pathways are downregulated after FcRn blockade in gMG.
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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 Socratic graph.