Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.

2.50
Hdl Handle:
http://hdl.handle.net/10033/615621
Title:
Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.
Authors:
Waffarn, Elizabeth E; Hastey, Christine J; Dixit, Neha; Soo Choi, Youn; Cherry, Simon; Kalinke, Ulrich ( 0000-0003-0503-9564 ) ; Simon, Scott I; Baumgarth, Nicole
Abstract:
Innate-like B-1a lymphocytes rapidly redistribute to regional mediastinal lymph nodes (MedLNs) during influenza infection to generate protective IgM. Here we demonstrate that influenza infection-induced type I interferons directly stimulate body cavity B-1 cells and are a necessary signal required for B-1 cell accumulation in MedLNs. Vascular mimetic flow chamber studies show that type I interferons increase ligand-mediated B-1 cell adhesion under shear stress by inducing high-affinity conformation shifts of surface-expressed integrins. In vivo trafficking experiments identify CD11b as the non-redundant, interferon-activated integrin required for B-1 cell accumulation in MedLNs. Thus, CD11b on B-1 cells senses infection-induced innate signals and facilitates their rapid sequester into secondary lymphoid tissues, thereby regulating the accumulation of polyreactive IgM producers at sites of infection.
Affiliation:
Twincore Centre of Experimental and Clinical Infection Research; a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover 30625, Germany.
Citation:
Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. 2015, 6:8991 Nat Commun
Journal:
Nature communications
Issue Date:
2015
URI:
http://hdl.handle.net/10033/615621
DOI:
10.1038/ncomms9991
PubMed ID:
26612263
Type:
Article
Language:
en
ISSN:
2041-1723
Appears in Collections:
Publications of the TwinCore unit experimental Infectionresearch(EXPI)

Full metadata record

DC FieldValue Language
dc.contributor.authorWaffarn, Elizabeth Een
dc.contributor.authorHastey, Christine Jen
dc.contributor.authorDixit, Nehaen
dc.contributor.authorSoo Choi, Younen
dc.contributor.authorCherry, Simonen
dc.contributor.authorKalinke, Ulrichen
dc.contributor.authorSimon, Scott Ien
dc.contributor.authorBaumgarth, Nicoleen
dc.date.accessioned2016-07-06T08:35:21Z-
dc.date.available2016-07-06T08:35:21Z-
dc.date.issued2015-
dc.identifier.citationInfection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. 2015, 6:8991 Nat Communen
dc.identifier.issn2041-1723-
dc.identifier.pmid26612263-
dc.identifier.doi10.1038/ncomms9991-
dc.identifier.urihttp://hdl.handle.net/10033/615621-
dc.description.abstractInnate-like B-1a lymphocytes rapidly redistribute to regional mediastinal lymph nodes (MedLNs) during influenza infection to generate protective IgM. Here we demonstrate that influenza infection-induced type I interferons directly stimulate body cavity B-1 cells and are a necessary signal required for B-1 cell accumulation in MedLNs. Vascular mimetic flow chamber studies show that type I interferons increase ligand-mediated B-1 cell adhesion under shear stress by inducing high-affinity conformation shifts of surface-expressed integrins. In vivo trafficking experiments identify CD11b as the non-redundant, interferon-activated integrin required for B-1 cell accumulation in MedLNs. Thus, CD11b on B-1 cells senses infection-induced innate signals and facilitates their rapid sequester into secondary lymphoid tissues, thereby regulating the accumulation of polyreactive IgM producers at sites of infection.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAnimalsen
dc.subject.meshAntigens, CD11ben
dc.subject.meshB-Lymphocyte Subsetsen
dc.subject.meshCell Adhesionen
dc.subject.meshCell Migration Assays, Leukocyteen
dc.subject.meshCell Movementen
dc.subject.meshFlow Cytometryen
dc.subject.meshImmunoglobulin Men
dc.subject.meshInfluenza A virusen
dc.subject.meshInterferon Type Ien
dc.subject.meshLymph Nodesen
dc.subject.meshMediastinumen
dc.subject.meshMiceen
dc.subject.meshOrthomyxoviridae Infectionsen
dc.subject.meshReal-Time Polymerase Chain Reactionen
dc.titleInfection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.en
dc.typeArticleen
dc.contributor.departmentTwincore Centre of Experimental and Clinical Infection Research; a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover 30625, Germany.en
dc.identifier.journalNature communicationsen

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