Evidence map›Paper›PMID 40107244›Full record

ArticleCell reports. Medicine2025

T-bet+ CXCR3+ B cells drive hyperreactive B-T cell interactions in multiple sclerosis.

Ivan Jelcic, Reza Naghavian, Imran Fanaswala, Will Macnair, Cinzia Esposito, Daniela Calini, Yanan Han, Zoe Marti, Catarina Raposo, Jacobo Sarabia Del Castillo and 17 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Single-Cell Profiling Reveals Clonally Expanded CX3CR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Comparative Effectiveness of Rituximab in Treatment-Naïve vs. Switch Patients with Multiple Sclerosis: A Real-World Retrospective Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  11. Investigations of remibrutinib in models pertinent to multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    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

27 authors.

Ivan JelcicNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Roche Pharma Research and Early Development (pRED), Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland. Electronic address: ivan.jelcic@roche.com.
Reza NaghavianNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland.
Imran FanaswalaSIB Swiss Institute of Bioinformatics, University of Zurich, Zurich, Switzerland; Department of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Will MacnairRoche Pharma Research and Early Development (pRED), Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Cinzia EspositoDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Daniela CaliniRoche Pharma Research and Early Development (pRED), Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Yanan HanDepartment of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Zoe MartiNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Cellerys AG, Schlieren, Switzerland.
Catarina RaposoRoche Pharma Research and Early Development (pRED), Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Jacobo Sarabia Del CastilloDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Pietro OldratiNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Cellerys AG, Schlieren, Switzerland.
Daniel ErnyNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Institute of Neuropathology, University of Freiburg, Freiburg, Germany.
Veronika KanaNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland.
Galina ZheleznyakovaDepartment of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Faiez Al NimerNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Björn TackenbergProduct Development Medical Affairs, Neuroscience and Rare Disease, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Ina ReichenNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland.
Mohsen KhademiDepartment of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Fredrik PiehlDepartment of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Mark D RobinsonSIB Swiss Institute of Bioinformatics, University of Zurich, Zurich, Switzerland; Department of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Ilijas JelcicNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland.
Mireia SospedraNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Cellerys AG, Schlieren, Switzerland.
Lucas PelkmansDepartment of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Dheeraj MalhotraRoche Pharma Research and Early Development (pRED), Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Richard ReynoldsDepartment of Brain Sciences, Imperial College, London, UK.
Maja JagodicDepartment of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Roland MartinNeuroimmunology and MS Research Section (NIMS), Neurology Clinic, University of Zurich, University Hospital Zurich, 8091 Zurich, Switzerland; Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland; Therapeutic Design Unit, Center for Molecular Medicine, Department of Clinical Neurosciences, Karolinska Institutet, Stockholm, Sweden; Cellerys AG, Schlieren, Switzerland. Electronic address: roland.martin@uzh.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). Self-peptide-dependent autoproliferation (AP) of B and T cells is a key mechanism in MS. Here, we show that pro-inflammatory B-T cell-enriched cell clusters (BTECs) form during AP and mirror features of a germinal center reaction. T-bet+CXCR3+ B cells are the main cell subset amplifying and sustaining their counterpart Th1 cells via interferon (IFN)-γ and are present in highly inflamed meningeal tissue. The underlying B cell activation signature is reflected by epigenetic modifications and receptor-ligand interactions with self-reactive T cells. AP+ CXCR3+ B cells show marked clonal evolution from memory to somatically hypermutated plasmablasts and upregulation of IFN-γ-related genes. Our data underscore a key role of T-bet+CXCR3+ B cells in the pathogenesis of MS in both the peripheral immune system and the CNS compartment, and thus they appear to be involved in both early relapsing-remitting disease and the chronic stage.

Indexed as

B-LymphocytesMeningesMultiple SclerosisReceptors, CXCR3T-bet Transcription FactorAdultAgedCell ProliferationFemaleHumansInterferon-gammaMaleMiddle AgedTh1 CellsYoung AdultCXCR3 protein, humanInterferon-gammaReceptors, CXCR3T-bet Transcription FactorTBX21 protein, humanautoproliferationautoreactivityB-T cell-enriched clustersBTECCXCR3hyperreactive B-T cell interactionIFN-gammameningesmultiple sclerosisself-peptidesT-bet+ B cellsT cells

Identifiers

PMID40107244
PMCPMC11970401

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Registered trials

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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 OpenQuestion graph.