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 language | English (US) |
|---|---|
| Article number | 8991 |
| Journal | Nature Communications |
| Volume | 6 |
| DOIs | |
| State | Published - Nov 27 2015 |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Chemistry(all)
- Physics and Astronomy(all)
Cite this
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 R; Kalinke, Ulrich; Simon, Scott I.; Baumgarth, Nicole.
In: Nature Communications, Vol. 6, 8991, 27.11.2015.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Infection-induced type i interferons activate CD11b on B-1 cells for subsequent lymph node accumulation
AU - Waffarn, Elizabeth E.
AU - Hastey, Christine J.
AU - Dixit, Neha
AU - Soo Choi, Youn
AU - Cherry, Simon R
AU - Kalinke, Ulrich
AU - Simon, Scott I.
AU - Baumgarth, Nicole
PY - 2015/11/27
Y1 - 2015/11/27
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84948669128&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84948669128&partnerID=8YFLogxK
U2 - 10.1038/ncomms9991
DO - 10.1038/ncomms9991
M3 - Article
C2 - 26612263
AN - SCOPUS:84948669128
VL - 6
JO - Nature Communications
JF - Nature Communications
SN - 2041-1723
M1 - 8991
ER -