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

Author

Listed:
  • Elizabeth E. Waffarn

    (Center for Comparative Medicine, University of California Davis
    The Graduate Group in Immunology, University of California Davis)

  • Christine J. Hastey

    (Center for Comparative Medicine, University of California Davis
    The Graduate Group in Microbiology, University of California Davis)

  • Neha Dixit

    (The Graduate Group in Immunology, University of California Davis
    University of California Davis)

  • Youn Soo Choi

    (Center for Comparative Medicine, University of California Davis
    The Graduate Group in Immunology, University of California Davis
    Present address: Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, San Diego, California 92037, USA.)

  • Simon Cherry

    (University of California Davis)

  • Ulrich Kalinke

    (TWINCORE, Centre for Experimental and Clinical Infection Research, Helmholtz-Centre for Infection Research, Hannover Medical School)

  • Scott I. Simon

    (University of California Davis)

  • Nicole Baumgarth

    (Center for Comparative Medicine, University of California Davis
    Microbiology and Immunology, University of California Davis)

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.

Suggested Citation

  • Elizabeth E. Waffarn & Christine J. Hastey & Neha Dixit & Youn Soo Choi & Simon Cherry & Ulrich Kalinke & Scott I. Simon & Nicole Baumgarth, 2015. "Infection-induced type I interferons activate CD11b on B-1 cells for subsequent lymph node accumulation," Nature Communications, Nature, vol. 6(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9991
    DOI: 10.1038/ncomms9991
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