Evidence map›Paper›PMID 32761407›Full record

ArticleActa neuropathologica2020

Inhibition of Bruton's tyrosine kinase interferes with pathogenic B-cell development in inflammatory CNS demyelinating disease.

Sebastian Torke, Roxanne Pretzsch, Darius Häusler, Philipp Haselmayer, Roland Grenningloh, Ursula Boschert, Wolfgang Brück, Martin S Weber

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% of its field
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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Predictive factors for the progression of multiple sclerosis: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Pooled it
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  9. Investigations of remibrutinib in models pertinent to multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Bruton Tyrosine Kinase in Lesions of Multiple Sclerosis and 3 of Its Models.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Article
  16. Beyond relapses: How BTK inhibitors are shaping the future of progressive MS treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
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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

8 authors at 5 institutions in 3 countries.

Sebastian TorkeInstitute of Neuropathology, University Medical Center, Göttingen, Germany.
Roxanne PretzschInstitute of Neuropathology, University Medical Center, Göttingen, Germany.
Darius HäuslerInstitute of Neuropathology, University Medical Center, Göttingen, Germany.
Philipp HaselmayerTranslational Innovation Platform Immunology, Merck KGaA, Darmstadt, Germany.
Roland GrenninglohEMD Serono Research and Development Institute, Inc., Billerica, MA, USA.
Ursula BoschertAres Trading S.A., An Affiliate of Merck Serono S.A., Eysins, Switzerland.
Wolfgang BrückInstitute of Neuropathology, University Medical Center, Göttingen, Germany.
Martin S WeberInstitute of Neuropathology, University Medical Center, Göttingen, Germany. martin.weber@med.uni-goettingen.de.
University of Göttingen · DEUniversitätsmedizin Göttingen · DEMerck (Germany) · DEMerck Serono (Switzerland) · CHOno Pharmaceutical (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-CD20-mediated B-cell depletion effectively reduces acute multiple sclerosis (MS) flares. Recent data shows that antibody-mediated extinction of B cells as a lasting immune suppression, harbors the risk of developing humoral deficiencies over time. Accordingly, more selective, durable and reversible B-cell-directed MS therapies are needed. We here tested inhibition of Bruton's tyrosine kinase (BTK), an enzyme centrally involved in B-cell receptor signaling, as the most promising approach in this direction. Using mouse models of MS, we determined that evobrutinib, the first BTK inhibiting molecule being developed, dose-dependently inhibited antigen-triggered activation and maturation of B cells as well as their release of pro-inflammatory cytokines. Most importantly, evobrutinib treatment functionally impaired the capacity of B cells to act as antigen-presenting cells for the development of encephalitogenic T cells, resulting in a significantly reduced disease severity in mice. In contrast to anti-CD20, BTK inhibition silenced this key property of B cells in MS without impairing their frequency or functional integrity. In conjunction with a recent phase II trial reporting that evobrutinib is safe and effective in MS, our mechanistic data highlight therapeutic BTK inhibition as a landmark towards selectively interfering with MS-driving B-cell properties.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsB-LymphocytesCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalHumansLymphocyte ActivationMiceMice, Inbred C57BLPiperidinesProtein Kinase InhibitorsPyrimidinesT-LymphocytesAgammaglobulinaemia Tyrosine KinaseevobrutinibPiperidinesProtein Kinase InhibitorsPyrimidinesB cellsBruton’s tyrosine kinaseBTKiEvobrutinibExperimental autoimmune encephalomyelitisMultiple sclerosisMyeloid cells

Identifiers

PMID32761407
PMCPMC7498502
OpenAlexW3047313223

What OpenQuestion holds

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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 OpenQuestion graph.