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Rockefeller University Press, Journal of Experimental Medicine, 9(206), p. 2037-2051, 2009

DOI: 10.1084/jem.20082818

Rockefeller University Press, Journal of Cell Biology, 5(186), p. i9-i9

DOI: 10.1083/jcb1865oia9

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Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection

Journal article published in 2009 by Caetano Reis e. Sousa, Matthew J. Robinson, Fabiola Osorio ORCID, Marcela Rosas, Rui P. Freitas, Edina Schweighoffer, J. Sjef Verbeek, Olaf Groß, J. SjefVerbeek, J. Sjef Verbeek, Jürgen Ruland, Victor Tybulewicz, Gordon D. Brown, Luis Ferreira Moita ORCID, Philip R. Taylor and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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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.