Evidence map›Paper›PMID 36854993›Full record

ArticleActa neuropathologica2023

IL-10-providing B cells govern pro-inflammatory activity of macrophages and microglia in CNS autoimmunity.

Anastasia Geladaris, Silke Häusser-Kinzel, Roxanne Pretzsch, Nitzan Nissimov, Klaus Lehmann-Horn, Darius Häusler, Martin S Weber

Open access · hybridFull text read
In one paragraph

Article in Acta neuropathologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.7field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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  11. Expansion of B10 cellsInternational journal of molecular medicine · 2025
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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

7 authors at 3 institutions in 1 country.

Anastasia Geladaris *Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany.
Silke Häusser-Kinzel *Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany.
Roxanne PretzschInstitute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany.
Nitzan NissimovInstitute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany.
Klaus Lehmann-HornDepartment of Neurology, School of Medicine, Technical University of Munich, Munich, Germany.
Darius Häusler *Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany.
Martin S Weber *Institute of Neuropathology, University Medical Centre Göttingen, Göttingen, Germany. martin.weber@med.uni-goettingen.de.ORCID 0000-0001-8409-0389
Fraunhofer Institute for Translational Medicine and Pharmacology · DEHumboldt-Universität zu Berlin · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B cells contribute to chronic inflammatory conditions as source of antibody-secreting plasma cells and as antigen-presenting cells activating T cells, making anti-CD20-mediated B cell depletion a widely used therapeutic option. B cells or B cell subsets may, however, exert regulatory effects, while to date, the immunological and/or clinical impact of these observations remained unclear. We found that in multiple sclerosis (MS) patients, B cells contain regulatory features and that their removal enhanced activity of monocytes. Using a co-culture system, we identified B cell-provided interleukin (IL)-10 as key factor in controlling pro-inflammatory activity of peripheral myeloid cells as well as microglia. Depleting B cells via anti-CD20 in a mouse model of MS unleashed the activity of myeloid cells and microglia and accelerated disease severity; in contrast, adoptive transfer of IL-10-providing B cells restored in vivo control of central nervous system (CNS) macrophages and microglia and reversed clinical exacerbation. These findings suggest that B cells exert meaningful regulatory properties, which should be considered when designing novel B cell-directed agents.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsAutoimmunityCentral Nervous SystemInterleukin-10MacrophagesMiceMice, Inbred C57BLMicrogliaIL10 protein, mouseInterleukin-10Experimental autoimmune encephalomyelitisInterleukin-10MicrogliaMultiple sclerosisMyeloid cellsRegulatory B cells

Identifiers

PMID36854993
PMCPMC10020302
OpenAlexW4322621096

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read76
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.