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

By Benjamin N. Gantner, Randi M. Simmons, Scott J. Canavera, Shizuo Akira, D. Underhill. Journal of Experimental Medicine, 2003

1,733 citations recorded by the source corpus.

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 β-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 κB by β-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 α. 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.

Subfields: Immunology, Microbiology

View Paper: https://www.semanticscholar.org/paper/5ef80580f1d5a8da826f2f2d89f74f8d2a4df1f0

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Citations in the corpus

Dectin-1: a signalling non-TLR pattern-recognition receptor (2006, background): “Some of these mechanisms, such as the respiratory burst , which leads to the production of reactive oxygen intermediates , are only induced by specific receptors, such as dectin-1 (Ref”
Dendritic cells: translating innate to adaptive immunity. (2006, background): “and DCs, binds yeast or zymosan particles but, in addition, dectin-1 associates with TLR-2 and thereby signals TNF-α and IL-12 production [86, 87].”
An integrated model of the recognition of Candida albicans by the innate immune system (2008, background): “Although Syk-dependent signalling from dectin 1 is sufficient for these responses, stimulation of the mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB pathways, with subsequent production of pro-inflammatory cytokines, such as tumour necrosis factor (TNF), requires collaborative si”
Dectin‐1 mediates macrophage recognition of Candida albicans yeast but not filaments (2005, methodology): “…recently demonstrated that, in macrophages and dendritic cells, Dectin-1 and Toll- like receptor 2 collaborate in coordinating inflammatory responses such as cytokine secretion and the production of reactive oxygen species (ROS) in response to b-glucan-containing particles (Gantner et al, 2003).”
CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”
Th17 cell differentiation: the long and winding road. (2008, positive): “b-glucan components in zymosan also signal through TLRindependent pathways to promote Th17 cell induction ( Gantner et al., 2003 ).”
Pathogen recognition and innate immunity. (2006, positive): “It has been demonstrated that dectin-1 can collaborate with TLR2 in response to yeast to elicit a strong inflammatory response via recruitment of the protein tyrosine kinase Syk (Gantner et al., 2003; Rogers et al., 2005; Underhill et al., 2005).”
DAMPening Inflammation by Modulating TLR Signalling (2010, background): “TLR2 was shown to collaborate with dectin-1 in zymosan recognition [70] or with the macrophage receptor with collagenous structure (MARCO) in addition to CD14 to respond to TDM, a cell wall glycolipid from Mycobacterium tuberculosis [71].”
The Role of TLR2 in Infection and Immunity (2012, neutral): “Dectin-1*** Aravalli et al. (2008) Zymosan** Saccharomyces cerevisiae TLR2/TLR6 CD14/dectin-1 Ikeda et al. (2008), Beutler et al. (2006), Gantner et al. (2003) Protozoan/helminth Glycosylphosphatidylinositol (GPI) anchors Trypanosoma, plasmodium, toxoplasma (protozoans) TLR2/TLR1**** and…”