The macrophage mannose receptor induces IL-17 in response to Candida albicans

The cytokine IL-17 controls neutrophil-mediated inflammatory responses. The pattern recognition receptor(s) that induce Th17 responses during infection, in the absence of artificial mitogenic stimulation with anti-CD3/anti-CD28 antibodies, remain obscure. We investigated the innate immune receptors...

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Published inCell host & microbe Vol. 5; no. 4; pp. 329 - 340
Main Authors van de Veerdonk, Frank L, Marijnissen, Renoud J, Kullberg, Bart Jan, Koenen, Hans J P M, Cheng, Shih-Chin, Joosten, Irma, van den Berg, Wim B, Williams, David L, van der Meer, Jos W M, Joosten, Leo A B, Netea, Mihai G
Format Journal Article
LanguageEnglish
Published United States 23.04.2009
Subjects
Candida albicans
Candida albicans - immunology
Cell Wall - immunology
Cells, Cultured
Humans
Interleukin-17 - biosynthesis
Lectins, C-Type - immunology
Macrophages - immunology
Mannans - immunology
Mannose-Binding Lectins - immunology
Membrane Proteins - immunology
Nerve Tissue Proteins - immunology
Receptors, Cell Surface - immunology
Toll-Like Receptor 2 - immunology
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Summary:The cytokine IL-17 controls neutrophil-mediated inflammatory responses. The pattern recognition receptor(s) that induce Th17 responses during infection, in the absence of artificial mitogenic stimulation with anti-CD3/anti-CD28 antibodies, remain obscure. We investigated the innate immune receptors and pathogen-associated molecular patterns involved in triggering Th17 responses during pathogen-specific host defense. The prototypic fungal pathogen Candida albicans was found to induce IL-17 more potently than Gram-negative bacteria. Candida mannan, but not zymosan, beta-glucans, Toll-like receptor (TLR) agonists, or the NOD2 ligand MDP, induced IL-17 production in the absence of anti-CD3/anti-CD28 antibodies. Candida-induced IL-17 response was dependent on antigen-presenting cells and the macrophage mannose receptor (MR), demonstrating that Candida mannan is not simply a mitogenic stimulus. The TLR2/dectin-1 pathway, but not TLR4 or NOD2, amplified MR-induced IL-17 production. This study identifies the specific pattern recognition receptors that trigger the Th17 response induced by a human pathogen in the absence of mitogenic stimulation.
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ISSN:1931-3128
1934-6069
DOI:10.1016/j.chom.2009.02.006