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Published in: Immunologic Research 6/2017

01-12-2017 | Original Article

Differences in innate IFNγ and IL-17 responses to Bordetella pertussis between BALB/c and C57BL/6 mice: role of γδT cells, NK cells, and dendritic cells

Authors: Yung-Yi C. Mosley, Fangjia Lu, Harm HogenEsch

Published in: Immunologic Research | Issue 6/2017

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Abstract

Cell-mediated immune responses characterized by the secretion of IFNγ and IL-17 play an important role in the immune response to Bordetella pertussis (B. pertussis). We investigated innate sources of IFNγ and IL-17 upon stimulation of spleen cells from BALB/c (B/c) and C57BL/6 (B6) mice with heat-killed B. pertussis (hkBp). Spleen cells from B/c mice secreted less IFNγ and more IL-17 than those from B6 mice. Innate IFNγ was produced predominantly by NK cells in B/c mice and by CD8 T cells and NK cells in B6 mice. Innate IL-17 was produced primarily by γδT cells in both mouse strains. The secretion of IFNγ was abrogated by anti-IL-12, and the production of IL-17 was abolished by anti-IL-1β- and anti-IL23-neutralizing antibodies. B/c dendritic cells (DCs) stimulated with hkBp secreted significantly more IL-1β and less IL-12 than B6 DCs. Differences in JNK phosphorylation in DCs suggest that this pathway plays a role in the differences between B/c and B6 strains. Mixed cultures of DCs and γδT cells from B/c and B6 showed that cytokines from DCs as well as γδT cell-intrinsic factors contributed to the robust innate IL-17 response in B/c strain. Stimulation of γδT cells with IL-1β and IL-23 was sufficient for IL-17 secretion whereas IL-12 inhibited the secretion of IL-17. A larger fraction of γδT cells were γδT-17 cells in B/c mice than B6 mice. Our data indicate important roles for genetically determined factors in the innate IFNγ and IL-17 responses to B. pertussis.
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Metadata
Title
Differences in innate IFNγ and IL-17 responses to Bordetella pertussis between BALB/c and C57BL/6 mice: role of γδT cells, NK cells, and dendritic cells
Authors
Yung-Yi C. Mosley
Fangjia Lu
Harm HogenEsch
Publication date
01-12-2017
Publisher
Springer US
Published in
Immunologic Research / Issue 6/2017
Print ISSN: 0257-277X
Electronic ISSN: 1559-0755
DOI
https://doi.org/10.1007/s12026-017-8957-4

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