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• W2110444822 endingPage "5639" @default.
• W2110444822 startingPage "5629" @default.
• W2110444822 abstract "Th cell responses induced by Aspergillus fumigatus have been extensively investigated in mouse models. However, the requirements for differentiation and the characteristics of A. fumigatus-induced human Th cell subsets remain poorly defined. We demonstrate that A. fumigatus induces Th1 and Th17 subsets in human PBMCs. Moreover, we show that the cytokine IL-22 is not restricted to a specific Th subset, in contrast to IL-17A. The pattern recognition and cytokine pathways that skew these Aspergillus-induced Th cell responses are TLR4- and IL-1-, IL-23-, and TNF-α-dependent. These pathways are of specific importance for production of the cytokines IL-17A and IL-22. Additionally, our data reveal that the dectin-1/Syk pathway is redundant and that TLR2 has an inhibitory effect on Aspergillus-induced IL-17A and IL-22 production. Notably, blocking complement receptor (CR)3 significantly reduced Aspergillus-induced Th1 and Th17 responses, and this was independent on the activation of the complement system. CR3 is a known receptor for β-1,3-glucan; however, blocking CR3 had significant effects on Th cell responses induced by heat-killed Aspergillus conidia, which have minimal β-glucan expression on their cell surface. Collectively, these data characterize the human Th cell subsets induced by Aspergillus, demonstrate that the capability to produce IL-22 is not restricted to a specific T cell subset, and provide evidence that CR3 might play a significant role in the adaptive host defense against Aspergillus, although the ligand and its action remain to be elucidated." @default.
• W2110444822 created "2016-06-24" @default.
• W2110444822 creator A5008373339 @default.
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• W2110444822 creator A5073302847 @default.
• W2110444822 creator A5075304288 @default.
• W2110444822 date "2013-05-03" @default.
• W2110444822 modified "2023-10-13" @default.
• W2110444822 title "<i>Aspergillus fumigatus</i>–Induced IL-22 Is Not Restricted to a Specific Th Cell Subset and Is Dependent on Complement Receptor 3" @default.
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• W2110444822 doi "https://doi.org/10.4049/jimmunol.1202601" @default.
• W2110444822 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23645883" @default.
• W2110444822 hasPublicationYear "2013" @default.
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