Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.
dc.contributor.author | Waffarn, Elizabeth E | |
dc.contributor.author | Hastey, Christine J | |
dc.contributor.author | Dixit, Neha | |
dc.contributor.author | Soo Choi, Youn | |
dc.contributor.author | Cherry, Simon | |
dc.contributor.author | Kalinke, Ulrich | |
dc.contributor.author | Simon, Scott I | |
dc.contributor.author | Baumgarth, Nicole | |
dc.date.accessioned | 2016-07-06T08:35:21Z | |
dc.date.available | 2016-07-06T08:35:21Z | |
dc.date.issued | 2015 | |
dc.identifier.citation | Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. 2015, 6:8991 Nat Commun | en |
dc.identifier.issn | 2041-1723 | |
dc.identifier.pmid | 26612263 | |
dc.identifier.doi | 10.1038/ncomms9991 | |
dc.identifier.uri | http://hdl.handle.net/10033/615621 | |
dc.description.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. | |
dc.language.iso | en | en |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.subject.mesh | Animals | en |
dc.subject.mesh | Antigens, CD11b | en |
dc.subject.mesh | B-Lymphocyte Subsets | en |
dc.subject.mesh | Cell Adhesion | en |
dc.subject.mesh | Cell Migration Assays, Leukocyte | en |
dc.subject.mesh | Cell Movement | en |
dc.subject.mesh | Flow Cytometry | en |
dc.subject.mesh | Immunoglobulin M | en |
dc.subject.mesh | Influenza A virus | en |
dc.subject.mesh | Interferon Type I | en |
dc.subject.mesh | Lymph Nodes | en |
dc.subject.mesh | Mediastinum | en |
dc.subject.mesh | Mice | en |
dc.subject.mesh | Orthomyxoviridae Infections | en |
dc.subject.mesh | Real-Time Polymerase Chain Reaction | en |
dc.title | Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. | en |
dc.type | Article | en |
dc.contributor.department | 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. | en |
dc.identifier.journal | Nature communications | en |
refterms.dateFOA | 2018-06-13T21:36:57Z | |
html.description.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. |