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

Elizabeth E. Waffarn, Christine J. Hastey, Neha Dixit, Youn Soo Choi, Simon R Cherry, Ulrich Kalinke, Scott I. Simon, Nicole Baumgarth

Research output: Contribution to journalArticle

23 Scopus citations

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.

Original languageEnglish (US)
Article number8991
JournalNature Communications
Volume6
DOIs
StatePublished - Nov 27 2015

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)

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