Evidence map›Paper›PMID 42624846›Full record

ArticleNature communications2026

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

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 and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Niels von Wardenburg *Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. niels.von-wardenburg@charite.de.ORCID http://orcid.org/0000-0003-0476-9813
Gregorio Spagni *German Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-0656-9671
S Momsen Reincke *Department of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-8132-3527
Stephanie WernickGerman Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany.
Hans-Christian KornauGerman Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-4187-7549
Viktoria ZinnowGerman Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany.
Amelya Keles SlevogtDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0001-5328-2740
Lucie Y LiDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0001-8098-1977
Marie A HomeyerDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Sonja BlumenauDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Maria StecklumExperimental Pharmacology and Oncology Berlin-Buch GmbH, Berlin, Germany.ORCID http://orcid.org/0009-0001-7951-5730
Dietmar SchmitzGerman Center for Neurodegenerative Diseases (DZNE) Berlin, Berlin, Germany.
Andreas PelzDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Valentina DamatoDepartment of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), University of Florence, Florence, Italy.
Nicholas SandersonNeurologic Clinic and Policlinic and Research Center for Clinical Neuroimmunology and Neuroscience, Departments of Medicine, Biomedicine, and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0003-1711-7275
Tobias DerfussNeurologic Clinic and Policlinic and Research Center for Clinical Neuroimmunology and Neuroscience, Departments of Medicine, Biomedicine, and Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland.
Minh C PhamDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0003-0234-4790
Kevin C O'ConnorDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-7056-419X
Andreas MeiselDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0001-7233-5342
Harald PrüssDepartment of Neurology with Experimental Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. harald.pruess@dzne.de.ORCID http://orcid.org/0000-0002-8283-7976

Funding

The Impact of COVID-19 on People Living with Rare Diseases and Their FamiliesU2CTR002818 · NCATS · CINCINNATI CHILDRENS HOSP MED CTR · PI Maurizio Macaluso, Michael Wagner · 2019 to 2026
$51.2M
Rare Disease Network for Myasthenia GravisU54NS115054 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI HENRY J KAMINSKI · 2019 to 2026
$11.9M
Mechanisms of autoimmunity in myasthenia gravisR01AI114780 · NIAID · YALE UNIVERSITY · PI Kevin C O'Connor · 2016 to 2026
$4.7M
Helmholtz Association HIL-A03NCATS NIH HHS U2C TR002818NIAID NIH HHS R01 AI114780NINDS NIH HHS U54 NS115054
6 · The paper itself

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.

Indexed as

AutoantibodiesB-LymphocytesMyasthenia GravisMyasthenia Gravis, Autoimmune, ExperimentalReceptors, Chimeric AntigenReceptors, CholinergicReceptors, NicotinicT-LymphocytesAnimalsDisease Models, AnimalFemaleHumansMiceNeuromuscular JunctionAutoantibodiesReceptors, Chimeric AntigenReceptors, CholinergicReceptors, Nicotinic

Identifiers

PMID42624846
PMCPMC13493945

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.