Journal
IMMUNITY
Volume 32, Issue 5, Pages 681-691Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2010.05.001
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Funding
- Japan Science and Technology Corporation
- Promotion of Basic Research Activities for Innovative Biosciences
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Health Science Research Grant for Research on Emerging and Re-emerging Infectious Diseases
- Ministry of Health, Labour, and Welfare of Japan
- Grants-in-Aid for Scientific Research [22700448] Funding Source: KAKEN
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Dectin-2 (gene symbol Clec4n) is a C-type lectin expressed by dendritic cells (DCs) and macrophages. However, its functional roles and signaling mechanisms remain to be elucidated. Here, we generated Clec4n(-/-) mice and showed that this molecule is important for host defense against Candida albicans (C. albicans). Clec4n(-/-) DCs had virtually no fungal alpha-mannan-induced cytokine production. Dectin-2 signaling induced cytokines through an FcR gamma chain and Syk-CARD9-NF-kappa B-dependent signaling pathway without involvement of MAP kinases. The yeast form of C. albicans induced interleukin-1 beta (IL-1 beta) and IL-23 secretion in a Dectin-2-dependent manner. In contrast, cytokine production induced by the hyphal form was only partially dependent on this lectin. Both yeast and hyphae induced Th17 cell differentiation, in which Dectin-2, but not Dectin-1, was mainly involved. Because IL-17A-deficient mice were highly susceptible to systemic candida infection, this study suggests that Dectin-2 is important in host defense against C. albicans by inducing Th17 cell differentiation.
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