Evidence map›Paper›PMID 41470000›Full record

ReviewJournal of neuroinflammation2025

CAR T cells as novel therapeutic strategy for multiple sclerosis and other neuroimmune disorders.

Sara Samadzadeh, Natalia Szejko, Yara Hamadah, Wan Ying Tan, Sanja Gluscevic, Vinícius Boldrini, Vito A G Ricigliano, Hans-Peter Hartung, Xavier Montalban, ECF Young Investigators/Fellows Initiative

Abstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Sara Samadzadeh *Experimental and Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt- Universität zu Berlin, Berlin, 12203, Germany.
Natalia Szejko *Department of Bioethics, Medical University of Warsaw, Warsaw, Poland. szejko.natalia@mh-hannover.de.
Yara HamadahDepartment of Internal Medicine, University of Connecticut School of Medicine, Farmington, CT, USA.
Wan Ying TanDepartment of Hematology & Oncology, Neag Comprehensive Cancer Center, University of Connecticut School of Medicine, Farmington, CT, USA.
Sanja GluscevicNeurology Clinic, Clinical Centre of Montenegro, Podgorica, 81000, Montenegro.
Vinícius BoldriniBrazilian Institute of Neuroscience and Neurotechnology (BRAINN), Department of Neurology, University of Campinas (UNICAMP), Campinas, São Paulo, Brazil.
Vito A G RiciglianoNeurology Unit, Paris Saclay Hospital, Orsay, France.
Hans-Peter HartungBrain and Mind Center, University of Sydney, Sydney, 2050, Australia.
Xavier MontalbanMultiple Sclerosis Centre of Catalonia (CEMCAT) and Department of Neurology, Hospital UniversitaryVall d´Hebron, Universitat Autonoma de Barcelona and Universitat de Vic/Central de Catalunya (UVic/UCC), Barcelona, Spain.
ECF Young Investigators/Fellows Initiative

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chimeric antigen receptor (CAR) T-cell therapy is rapidly emerging as a transformative approach for treating multiple sclerosis (MS) and other neuroimmune disorders such as neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and myasthenia gravis (MG), alongside several other rare neuroimmunological conditions currently being evaluated in compassionate-use or early-phase studies. These conditions are driven in part by autoreactive B cells that sustain chronic inflammation and progressive tissue damage. While current immunomodulatory therapies have improved clinical outcomes, they often require lifelong administration and fail to effectively eliminate compartmentalized inflammation within the central nervous system. Recent advances in CD19- and BCMA-directed CAR T-cell therapy, initially developed for hematologic malignancies, demonstrate the potential to achieve targeted, durable B-cell depletion and immune reprogramming in autoimmune diseases. Preclinical models and early-phase clinical trials have shown promising efficacy, including reduced relapse rates, stabilization of disability progression, and decreased autoantibody levels, alongside a favorable safety profile with lower rates of high-grade cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) compared to oncologic applications. This review synthesizes the current evidence supporting the use of CAR T-cell therapy in neuroinflammatory diseases and explores its potential to redefine treatment paradigms by shifting from chronic immunosuppression to long-term immune tolerance, creating a favorable environment for repair mechanisms. Realizing the full therapeutic promise of CAR T-cells in autoimmune neurology will require sustained research in heterogeneous populations and across disease spectrums.

Indexed as

Immunotherapy, AdoptiveMultiple SclerosisReceptors, Chimeric AntigenT-LymphocytesAnimalsHumansReceptors, Chimeric AntigenAutoimmune disordersAutoimmune neurologyB cellsChimeric antigen receptor t cellsImmunotherapyMultiple sclerosisNeuroinflammation

Identifiers

PMID41470000
PMCPMC12837059

What OpenQuestion holds

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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 OpenQuestion graph.