The macrophage mannose receptor induces IL-17 in response to Candida albicans.
until further notice
SourceCell Host & Microbe, 5, 4, (2009), pp. 329-340
Article / Letter to editor
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Blood Transfusion and Transplantation Immunology
Laboratory of Medical Immunology
Cell Host & Microbe
SubjectN4i 2: Invasive mycoses and compromised host; N4i 4: Auto-immunity, transplantation and immunotherapy; NCMLS 1: Infection and autoimmunity; NCMLS 2: Immune Regulation
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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