Evidence map›Paper›PMID 27396388›Full record

ArticleNature communications2016

Treatment of ongoing autoimmune encephalomyelitis with activated B-cell progenitors maturing into regulatory B cells.

Sarantis Korniotis, Christophe Gras, Hélène Letscher, Ruddy Montandon, Jérôme Mégret, Stefanie Siegert, Sophie Ezine, Padraic G Fallon, Sanjiv A Luther, Simon Fillatreau and 1 more

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

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  19. Phenotypic identification of CD19Archives of medical science : AMS · 2019
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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

11 authors at 3 institutions in 4 countries.

Sarantis KorniotisInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Christophe GrasInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Hélène LetscherInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Ruddy MontandonInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Jérôme MégretUniversité Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Site Necker, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Stefanie SiegertDepartment of Biochemistry, University of Lausanne, Epalinges 1066, Switzerland.
Sophie EzineInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Padraic G FallonDepartment of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.
Sanjiv A LutherDepartment of Biochemistry, University of Lausanne, Epalinges 1066, Switzerland.
Simon FillatreauInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.
Flora ZavalaInstitut Necker Enfants Malades, Immunology, Infectiology and Haematology Department, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431, Paris 75014, France.ORCID 0000-0002-2338-6802
Délégation Paris 5 · FRUniversity of Lausanne · CHTrinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influence of signals perceived by immature B cells during their development in bone marrow on their subsequent functions as mature cells are poorly defined. Here, we show that bone marrow cells transiently stimulated in vivo or in vitro through the Toll-like receptor 9 generate proB cells (CpG-proBs) that interrupt experimental autoimmune encephalomyelitis (EAE) when transferred at the onset of clinical symptoms. Protection requires differentiation of CpG-proBs into mature B cells that home to reactive lymph nodes, where they trap T cells by releasing the CCR7 ligand, CCL19, and to inflamed central nervous system, where they locally limit immunopathogenesis through interleukin-10 production, thereby cooperatively inhibiting ongoing EAE. These data demonstrate that a transient inflammation at the environment, where proB cells develop, is sufficient to confer regulatory functions onto their mature B-cell progeny. In addition, these properties of CpG-proBs open interesting perspectives for cell therapy of autoimmune diseases.

Indexed as

Bone Marrow TransplantationAnimalsB-Lymphocytes, RegulatoryCell DifferentiationCell MovementChemokine CCL19Encephalomyelitis, Autoimmune, ExperimentalFemaleInterferon-gammaInterleukin-10Lymph NodesMice, Inbred C57BLOligodeoxyribonucleotidesPrecursor Cells, B-LymphoidCcl19 protein, mouseChemokine CCL19CPG 10101IL10 protein, mouseInterferon-gammaInterleukin-10Oligodeoxyribonucleotides

Identifiers

PMID27396388
PMCPMC4942579
OpenAlexW2465454048

What OpenQuestion holds

Textmetadata
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.