The Journal of Experimental Medicine
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Published online 28 April 2003 doi:10.1084/jem.20021787
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© Rockefeller University Press, 0022-1007/2003/5/1107 $5.00
The Journal of Experimental Medicine, Volume 197, Number 9, 1107-1117

Collaborative Induction of Inflammatory Responses by Dectin-1 and Toll-like Receptor 2

Benjamin N. Gantner1, Randi M. Simmons2, Scott J. Canavera1, Shizuo Akira3 and David M. Underhill2

1 Department of Immunology, University of Washington, Seattle, WA 98105
2 Institute for Systems Biology, Seattle, WA 98103
3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan

Address correspondence to David M. Underhill, Institute for Systems Biology, 1441 N. 34th Street, Seattle, WA 98103. Phone: 206-732-1374; Fax: 206-732-1299; E-mail: dunderhill{at}systemsbiology.org

Toll-like receptors (TLRs) mediate recognition of a wide range of microbial products including lipopolysaccharides, lipoproteins, flagellin, and bacterial DNA, and signaling through TLRs leads to the production of inflammatory mediators. In addition to TLRs, many other surface receptors have been proposed to participate in innate immunity and microbial recognition, and signaling through some of these receptors is likely to cooperate with TLR signaling in defining inflammatory responses. In this report we have examined how dectin-1, a lectin family receptor for ß-glucans, collaborates with TLRs in recognizing microbes. Dectin-1, which is expressed at low levels on macrophages and high levels on dendritic cells, contains an immunoreceptor tyrosine-based activation motif–like signaling motif that is tyrosine phosphorylated upon activation. The receptor is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G–opsonized particles. Dectin-1 expression enhances TLR-mediated activation of nuclear factor {kappa}B by ß-glucan–containing particles, and in macrophages and dendritic cells dectin-1 and TLRs are synergistic in mediating production of cytokines such as interleukin 12 and tumor necrosis factor {alpha}. Additionally, dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by TLR activation. The data demonstrate that collaborative recognition of distinct microbial components by different classes of innate immune receptors is crucial in orchestrating inflammatory responses.

Key Words: lectin • ITAM • zymosan • dendritic cell • macrophage


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