Bispecific chimeric autoantibody receptor T cells eliminate acetylcholine receptor-specific B cells in myasthenia gravis models.

Authors

Niels von Wardenburg, Gregorio Spagni, S Momsen Reincke, Stephanie Wernick, Hans-Christian Kornau, Viktoria Zinnow, Amelya Keles Slevogt, Lucie Y Li, Marie A Homeyer, Sonja Blumenau, Maria Stecklum, Dietmar Schmitz, Andreas Pelz, Valentina Damato, Nicholas Sanderson, Tobias Derfuss, Minh C Pham, Kevin C O'Connor, Andreas Meisel, Harald Prüss

Published in

Nature communications. Volume 17. Issue 1. Aug 20, 2026. Epub Aug 20, 2026.

Abstract

Myasthenia gravis (MG) is an autoimmune neuromuscular disorder mediated by autoantibodies targeting the nicotinic acetylcholine receptor (nAChR), which can lead to severe disability and life-threatening crises. Current therapies rely on broad immunosuppression and fail to achieve sustained remission in the majority of patients. Here, we report the development of AChR chimeric autoantibody receptor (CAAR) T cells engineered to selectively eliminate autoreactive B cells producing anti-AChR autoantibodies. T cells were co-transduced with CAARs expressing extracellular domains of the AChRα1 or β1 subunits, enabling recognition of a broad range of pathogenic antibodies. AChR CAAR T cells selectively secreted effector cytokines upon activation, and efficiently lysed target cells. In a xenograft mouse model, they depleted pathogenic B cell lines and reduced autoantibody levels in the circulation and at the neuromuscular junction. These findings establish AChR CAAR T cells as a precision immunotherapy with the potential to achieve durable remission in refractory MG.

PMID:
42624846
Bibliographic data and abstract were imported from PubMed on 21 Aug 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.