title: Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.
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.
authors.affiliation: Center for Comparative Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA.|The Graduate Group in Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Elizabeth E
authors.initials: EE
authors.lastname: Waffarn
authors.affiliation: Center for Comparative Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA.|The Graduate Group in Microbiology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Christine J
authors.initials: CJ
authors.lastname: Hastey
authors.affiliation: The Graduate Group in Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.|Department of Biomedical Engineering, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Neha
authors.initials: N
authors.lastname: Dixit
authors.affiliation: Center for Comparative Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA.|The Graduate Group in Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Youn
authors.initials: Y
authors.lastname: Soo Choi
authors.affiliation: Department of Biomedical Engineering, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Simon
authors.initials: S
authors.lastname: Cherry
authors.affiliation: TWINCORE, Centre for Experimental and Clinical Infection Research, Helmholtz-Centre for Infection Research, Hannover Medical School, 7 Feodor-Lynen Strasse, Hannover 30625, Germany.
authors.forename: Ulrich
authors.initials: U
authors.lastname: Kalinke
authors.affiliation: Department of Biomedical Engineering, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Scott I
authors.initials: SI
authors.lastname: Simon
authors.affiliation: Center for Comparative Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA.|Department of Pathology, Microbiology and Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
authors.forename: Nicole
authors.initials: N
authors.lastname: Baumgarth
mesh_terms: D000818:Animals; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D039481:CD11b Antigen / Q000276:immunology*; D002448:Cell Adhesion / Q000276:immunology*; D054441:Cell Migration Assays, Leukocyte; D002465:Cell Movement / Q000276:immunology*; D005434:Flow Cytometry; D007075:Immunoglobulin M / Q000276:immunology*; D009980:Influenza A virus; D007370:Interferon Type I / Q000276:immunology*; D008198:Lymph Nodes / Q000276:immunology*; D008482:Mediastinum; D051379:Mice; D009976:Orthomyxoviridae Infections / Q000276:immunology*; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D039481:CD11b Antigen; D007075:Immunoglobulin M; D007370:Interferon Type I