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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.
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
refterms.dateFOA2018-06-13T21:36:57Z
html.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.


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