dc.contributor.author
Korniotis, Sarantis
dc.contributor.author
Gras, Christophe
dc.contributor.author
Letscher, Helene
dc.contributor.author
Montandon, Ruddy
dc.contributor.author
Megret, Jerome
dc.contributor.author
Siegert, Stefanie
dc.contributor.author
Ezine, Sophie
dc.contributor.author
Fallon, Padraic G.
dc.contributor.author
Luther, Sanjiv A.
dc.contributor.author
Fillatreau, Simon
dc.contributor.author
Zavala, Flora
dc.date.accessioned
2018-06-08T02:51:55Z
dc.date.available
2016-09-02T09:46:07.347Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/14017
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-18214
dc.description.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.
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Treatment of ongoing autoimmune encephalomyelitis with activated B-cell
progenitors maturing into regulatory B cells
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Nature Communications. - 7 (2015), Artikel Nr. 12134
dcterms.bibliographicCitation.doi
10.1038/ncomms12134
dcterms.bibliographicCitation.url
http://www.nature.com/ncomms/2016/160711/ncomms12134/full/ncomms12134.html
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000025143
refubium.note.author
Der Artikel wurde in einer Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000006899
dcterms.accessRights.openaire
open access