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Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation.
Waffarn, Elizabeth E Hastey, Christine J Dixit, Neha Soo Choi, Youn Cherry, Simon Simon, Scott I Baumgarth, Nicole
Waffarn, Elizabeth E
Hastey, Christine J
Dixit, Neha
Soo Choi, Youn
Cherry, Simon
Simon, Scott I
Baumgarth, Nicole
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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.
Citation
Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation. 2015, 6:8991 Nat Commun
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PubMed ID
PubMed Central ID
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Article
Language
en
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Series/Report no.
ISSN
2041-1723