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- W2174391106 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." @default.
- W2174391106 created "2016-06-24" @default.
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- W2174391106 date "2015-11-27" @default.
- W2174391106 modified "2023-10-13" @default.
- W2174391106 title "Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation" @default.
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- W2174391106 doi "https://doi.org/10.1038/ncomms9991" @default.
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