Fig. 6

Scheme summarizing the single-hit mechanism of IL-1β secretion by steady-state DCs exposed to food-grade SAS particles. In immature DCs, pro-IL-1β is not expressed, but its induction takes place upon uptake of SAS particles into endosomes and MyD88-dependent TLR signaling. Cleavage of the newly expressed pro-IL-1β precursor by the inflammasome-associated caspase leads to IL-1β secretion. In addition, the immature DCs undergo maturation involving shifts in multiple surface markers. IL-1β secretion in response to SAS particles is suppressed by cytochalasin or rottlerin (inhibitors of actin-dependent macropinocytosis), by chloroquine or bafilomycin A (inhibitors of endosomal TLR activation), by genetic ablation of MyD88 (the central adapter of TLR signaling) and by Z-VAD (an inhibitor of the inflammasome-associated caspase)