Abstract
Innate immune cells detect pathogens via pattern recognition receptors (PRRs), which signal for initiation of immune responses to infection. Studies with Dectin-1, a PRR for fungi, have defined a novel innate signaling pathway involving Syk kinase and the adaptor CARD9, which is critical for inducing Th17 responses to fungal infection. We show that another C-type lectin, Dectin-2, also signals via Syk and CARD9, and contributes to dendritic cell (DC) activation by fungal particles. Unlike Dectin-1, Dectin-2 couples to Syk indirectly, through association with the FcRgamma chain. In a model of Candida albicans infection, blockade of Dectin-2 did not affect innate immune resistance but abrogated Candida-specific T cell production of IL-17 and, in combination with the absence of Dectin-1, decreased Th1 responses to the organism. Thus, Dectin-2 constitutes a major fungal PRR that can couple to the Syk-CARD9 innate signaling pathway to activate DCs and regulate adaptive immune responses to fungal infection.
Original language | English |
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Pages (from-to) | 2037-2051 |
Number of pages | 15 |
Journal | Journal of Experimental Medicine |
Volume | 206 |
Issue number | 9 |
DOIs | |
Publication status | Published - 31 Aug 2009 |
Keywords
- adaptor proteins, signal transducing
- adaptor proteins, vesicular transport
- animals
- candidiasis
- flow cytometry
- immunoblotting
- interleukin-17
- intracellular signaling peptides and proteins
- lectins, C-type
- mice
- mice, inbred C57BL
- mice, knockout
- myeloid differentiation factor 88
- protein-tyrosine kinases
- receptors, pattern recognition
- reverse transcriptase polymerase chain reaction
- signal transduction
- t-lymphocytes, helper-inducer