Evidence map›Paper›PMID 42069653›Full record

ArticleJournal of neuroinflammation2026

Impaired suppressive effect of FoxP3 regulatory T cells on B cells in multiple sclerosis.

Viktoria B Greeck, Cornelia Würthwein, Karina Mimura, Katharina Mattes, Michael Kutza, Lucas Schirmer, Richard Fairless, Sarah K Williams, Sven Jarius, Jürgen Haas and 2 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 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

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

12 authors.

Viktoria B Greeck *Division of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Cornelia Würthwein *Division of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Karina Mimura *Division of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Katharina MattesDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Michael KutzaDivision of Neuroimmunology, Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Lucas SchirmerInterdisciplinary Center for Neurosciences (IZN), Heidelberg University, Heidelberg, Germany.
Richard FairlessDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Sarah K WilliamsDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Sven JariusDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Jürgen HaasDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Klemens RuprechtDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Brigitte WildemannDivision of Neuroimmunology, Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. brigitte.wildemann@med.uni-heidelberg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundB cells are key contributors to the pathogenesis of many autoimmune diseases (AID), including multiple sclerosis (MS), and appear to evade the peripheral tolerance checkpoints that normally maintain immune homeostasis. The fate of B cells at these checkpoints is believed to be regulated by intracellular Ca

objectiveTo assess the ability of Tregs to suppress activated B cells in healthy individuals and patients with MS.

methodsB and T cell populations were isolated from 40 MS patients and 98 age- and sex-matched healthy donors (HD). Single-cell live Ca²⁺ imaging was used to assess early activation signals in B cells. In vitro proliferation assays and coculture experiments were employed to evaluate downstream responses, including proliferation, transcription factor activation (NFATc1, NF-ĸB), interleukin 6 (IL-6) release, and surface expression levels of antigen-presenting capacity (APC) markers both in anti-IgM/anti-CD40-stimulated B cells alone, and in the presence of Tregs.

resultsWe demonstrate that Tregs exert a robust suppressive effect on B cell proliferation, IL-6 secretion and NFATc1 which is [1] independent of Ca

conclusionThis study provides new data on Treg-mediated suppression of B cells in humans, including at single-cell level. Our findings show that the Treg dysfunction in MS previously described in the context of Tcon regulation extends to B cell regulation. Given the critical role of B cells in MS pathogenesis, this impaired Treg-B cell interaction may represent a previously underappreciated disease mechanism with potentially important therapeutic implications.

Indexed as

B-LymphocytesForkhead Transcription FactorsMultiple SclerosisT-Lymphocytes, RegulatoryAdultCalciumCell ProliferationCells, CulturedCoculture TechniquesFemaleHumansMaleMiddle AgedNFATC Transcription FactorsCalciumForkhead Transcription FactorsFOXP3 protein, humanNFATC Transcription FactorsAPC markersB cell receptorB cellsCalcium signalingHealthy donorsInterleukin 6Multiple sclerosisNFATc1NF-κBProliferationRegulatory T cells (Tregs)Single-cell analysisTranscriptome

Identifiers

PMID42069653
PMCPMC13179635

What Socratic holds

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LicenceCC BY
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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 Socratic graph.