Abstract
Abstract Dendritic cells (DCs) can induce and control host immune responses. DC subset-dependent functional specialties and their ability to display functional plasticity, which is mainly driven by signals via pattern-recognition receptors (PRRs), identify DCs as immune orchestrators. A PRR, Dectin-1 is expressed on myeloid DCs (mDCs) and is known to play an important role in TH17 responses. Here, we demonstrate that human plasmacytoid DCs (pDCs) express Dectin-1. Interestingly, Dectin-1-activated pDCs promote TH2 induction and activation, whereas Dectin-1-activated mDCs decrease both. This counter-regulation of TH2 by the two DC subsets is mainly due to their distinct abilities to control OX40L expression through different mechanisms. This study provides new insights for the regulation of host immune responses by DCs during microbial infections.
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