Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE RESEARCH
DOI: 10.1038/ncomms9991
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Funding
- NIH [AI051354, AI085568, U19AI109962, AI047294, T32OD010931, T35-OD010956]
- University of California, Davis, through pilot grant from the Committee on Research
- School of Veterinary Medicine, UC Davis
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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.
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