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Nat Commun. 2015 Nov 27;6:8991. doi: 10.1038/ncomms9991.

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

Author information

1
Center for Comparative Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
2
The Graduate Group in Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
3
The Graduate Group in Microbiology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
4
Department of Biomedical Engineering, University of California Davis, One Shields Avenue, Davis, California 95616, USA.
5
TWINCORE, Centre for Experimental and Clinical Infection Research, Helmholtz-Centre for Infection Research, Hannover Medical School, 7 Feodor-Lynen Strasse, Hannover 30625, Germany.
6
Department of Pathology, Microbiology and Immunology, University of California Davis, One Shields Avenue, Davis, California 95616, USA.

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.

PMID:
26612263
PMCID:
PMC4896500
DOI:
10.1038/ncomms9991
[Indexed for MEDLINE]
Free PMC Article

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