Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 2, Pages 662-666Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002725
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Funding
- INSERM [R04193KS]
- Fondation pour la Recherche Medicale [INE20051105133]
- Agence Nationale de Recherches [R07119KS]
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We have shown previously that peripheral lymph node-resident retinoic acid receptor-related orphan receptor gamma t(+) NK1.1(-) invariant NKT (iNKT) cells produce IL-17A independently of IL-6. In this study, we show that the concomitant presence of IL-1 and IL-23 is crucial to induce a rapid and sustained IL-17A/F and IL-22 response by these cells that requires TCR-CD1d interaction and partly relies on IL-23-mediated upregulation of IL-23R and IL-1R1 expression. We further show that IL-1 and IL-23 produced by pathogen-associated molecular pattern-stimulated dendritic cells induce this response from NK1.1(-) iNKT cells in vitro, involving mainly TLR2/4-signaling pathways. Finally, we found that IL-17A production by these cells occurs very early and transiently in vivo in response to heat-killed bacteria. Overall, our study indicates that peripheral lymph node NK1.1(-) iNKT cells could be a source of innate Th17-related cytokines during bacterial infections and supports the hypothesis that they are able to provide an efficient first line of defense against bacterial invasion. The Journal of Immunology, 2011, 186: 662-666.
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