Evidence map›Paper›PMID 38134930›Full record

ArticleCell reports. Medicine2024

B cell depletion attenuates CD27 signaling of T helper cells in multiple sclerosis.

Can Ulutekin, Edoardo Galli, Bettina Schreiner, Mohsen Khademi, Ilaria Callegari, Fredrik Piehl, Nicholas Sanderson, Daniel Kirschenbaum, Sarah Mundt, Massimo Filippi and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Observational
  2. Article
  3. Article
  4. CD56Clinical & translational immunology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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  12. Twin study dissects CXCR3Med (New York, N.Y.) · 2024
    Article
  13. Article
  14. Article
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

15 authors at 4 institutions in 3 countries.

Can UlutekinInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Edoardo GalliInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Multiple Sclerosis Center, Neurologic Clinic and Policlinic, Department of Biomedicine and Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland.
Bettina SchreinerInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Department of Neurology, University Hospital Zurich, Rämistrasse 100, 8091 Zurich, Switzerland.
Mohsen KhademiNeuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, Visionsgatan 18A, 171 76 Stockholm, Sweden.
Ilaria CallegariMultiple Sclerosis Center, Neurologic Clinic and Policlinic, Department of Biomedicine and Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland.
Fredrik PiehlNeuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, Visionsgatan 18A, 171 76 Stockholm, Sweden.
Nicholas SandersonMultiple Sclerosis Center, Neurologic Clinic and Policlinic, Department of Biomedicine and Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland.
Daniel KirschenbaumInstitute of Neuropathology, University Hospital Zurich, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.
Sarah MundtInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Massimo FilippiNeurology Unit, Neurorehabilitation Unit, Neurophysiology Service, and Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Via Olgettina n. 60 - 20132, Italy; Vita-Salute San Raffaele University, Milan, Via Olgettina n. 60 - 20132, Italy.
Roberto FurlanClinical Neuroimmunology Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina n. 60 - 20132, Milan, Italy.
Tomas OlssonNeuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, Visionsgatan 18A, 171 76 Stockholm, Sweden.
Tobias DerfussMultiple Sclerosis Center, Neurologic Clinic and Policlinic, Department of Biomedicine and Research Center for Clinical Neuroimmunology and Neuroscience Basel, University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland.
Florian IngelfingerInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Burkhard BecherInstitute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland. Electronic address: becher@immunology.uzh.ch.
University of Zurich · CHUniversity of Basel · CHKarolinska Institutet · SEVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis is a chronic inflammatory disease of the central nervous system. Whereas T cells are likely the main drivers of disease development, the striking efficacy of B cell-depleting therapies (BCDTs) underscore B cells' involvement in disease progression. How B cells contribute to multiple sclerosis (MS) pathogenesis-and consequently the precise mechanism of action of BCDTs-remains elusive. Here, we analyze the impact of BCDTs on the immune landscape in patients with MS using high-dimensional single-cell immunophenotyping. Algorithm-guided analysis reveals a decrease in circulating T follicular helper-like (Tfh-like) cells alongside increases in CD27 expression in memory T helper cells and Tfh-like cells. Elevated CD27 indicates disrupted CD27/CD70 signaling, as sustained CD27 activation in T cells leads to its cleavage. Immunohistological analysis shows CD70-expressing B cells at MS lesion sites. These results suggest that the efficacy of BCDTs may partly hinge upon the disruption of Th cell and B cell interactions.

Indexed as

Multiple SclerosisB-LymphocytesHumansImmunophenotypingSignal TransductionT-Lymphocytes, Helper-InducerB cell depletionCD27CD4(+) T cellsCD70mass cytometrymultiple sclerosis

Identifiers

PMID38134930
PMCPMC10829729
OpenAlexW4390064037

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.