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 Cherry, Ulrich Kalinke, Scott I. Simon and Nicole Baumgarth ()
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Elizabeth E. Waffarn: Center for Comparative Medicine, University of California Davis
Christine J. Hastey: Center for Comparative Medicine, University of California Davis
Neha Dixit: The Graduate Group in Immunology, University of California Davis
Youn Soo Choi: Center for Comparative Medicine, University of California Davis
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

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms9991

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