Dual Signaling of MyD88 and TRIF Is Critical for Maximal TLR4-Induced Dendritic Cell Maturation

摘要: TLR4 is a unique TLR because downstream signaling occurs via two separate pathways, as follows: MyD88 and Toll IL-1 receptor (TIR) domain-containing adaptor-inducing IFN-β (TRIF). In this study, we compared contrasted the interplay of these pathways between murine dendritic cells (DCs) macrophages during LPS stimulation. During activation, neither pathway on its own was critical for up-regulation costimulatory molecules in DCs, whereas largely TRIF dependent macrophages. LPS-induced secreted factors, which type I IFNs were one active components, played larger role promoting than DCs. both cell types, together accounted inflammatory response to activation. Furthermore, adaptors allowed maximal T priming by LPS-matured with playing TRIF. sum, our experimental systems, plays more important macrophage activation DC