ArticleScience advances2025
Composition and function of AChR chimeric autoantibody receptor T cells for antigen-specific B cell depletion in myasthenia gravis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed.
- Bispecific chimeric autoantibody receptor T cells eliminate acetylcholine receptor-specific B cells in myasthenia gravis models.Nature communications · 2026Article
- CAR T cell therapy beyond cancer: current status, challenges and future prospects.Signal transduction and targeted therapy · 2026Review
- Chimeric Antigen Receptor T-Cells in Myasthenia Gravis: Advances, Safety Challenges, and Future Directions.Muscle & nerve · 2026Review
- The Evolving Landscape of CAR T-Cell Therapy in Autoimmune Diseases: A State-of-the-Art Review (2025).Clinical reviews in allergy & immunology · 2026Review
- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
- Clinical progress of engineered cellular immunotherapies for autoimmunity.Nature biotechnology · 2026Review
- Engineered Bi-Specific AChR CAAR T Cells for Selective Elimination of Myasthenia Gravis B Cells.Research square · 2026Article
- Preclinical evaluation of antigen-specific B-cell depletion for phospholipase A2 receptor membranous nephropathy with chimeric autoantibody receptor T cells.Kidney international · 2026Article
- Chimeric antigen receptor technology: an emerging translational immunotherapy in nonneoplastic diseases.Frontiers in immunology · 2026Review
- Chimeric antigen receptor (CAR) therapies for precise eradication of pathogenic cells in autoimmunity.Arthritis research & therapy · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
In acetylcholine receptor (AChR)-seropositive myasthenia gravis (MG), anti-AChR autoantibodies impair neuromuscular transmission and cause severe muscle weakness. MG therapies broadly suppress immune function, risking infections. We designed a chimeric autoantibody receptor (CAAR) expressing the 210-amino acid extracellular domain of the AChR α subunit (A210) linked to CD137-CD3ζ cytoplasmic domains to direct T cell cytotoxicity against anti-AChRα B cells. A210-CAART incorporating a CD8α transmembrane domain (TMD8α) showed functional but unstable surface expression, partially restored by inhibiting lysosomal degradation. A210-CAART with a CD28 TMD showed sustained surface expression, independent of TMD dimerization motifs. In a mouse xenograft model, A210.TMD8α-CAART demonstrated early control of anti-AChR B cell outgrowth but subsequent rebound and loss of surface CAAR expression, whereas A210.TMD28-CAART induced sustained surface CAAR expression and target cell elimination. This study demonstrates the importance of the CD28 TMD for CAAR stability and in vivo function, laying the groundwork for future development of precision cellular immunotherapy for AChR-MG.
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