期刊
NATURE IMMUNOLOGY
卷 8, 期 6, 页码 630-638出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1460
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- MRC [MC_U117527252] Funding Source: UKRI
- Medical Research Council [MC_U117527252] Funding Source: Medline
- Swiss National Science Foundation [106884] Funding Source: Medline
- Wellcome Trust [086558] Funding Source: Medline
- Medical Research Council [MC_U117527252] Funding Source: researchfish
The C-type lectin dectin-1 binds to yeast and signals through the kinase Syk and the adaptor CARD9 to induce production of interleukin 10 (IL-10) and IL-2 in dendritic cells (DCs). However, whether this pathway promotes full DC activation remains unclear. Here we show that dectin-1-Syk-CARD9 signaling induced DC maturation and the secretion of proinflammatory cytokines, including IL-6, tumor necrosis factor and IL-23, but little IL-12. Dectin-1-activated DCs 'instructed' the differentiation of CD4+ IL-17-producing effector T cells (TH-17 cells) in vitro, and a dectin-1 agonist acted as an adjuvant promoting the differentiation of TH-17 and T helper type 1 cells in vivo. Infection with Candida albicans induced CARD9-dependent TH-17 responses to the organism. Our data indicate that signaling through Syk and CARD9 can couple innate to adaptive immunity independently of Toll-like receptor signals and that CARD9 is required for the development of TH-17 responses to some pathogens.
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