Toll-like receptor 2 (TLR2) and TLR4 differentially activate human dendritic cells.

摘要: Toll-like receptors (TLRs) mediate cell activation by various microbial products. Here, we demonstrate that of dendritic cells TLR2 or TLR4 agonists, although it led to comparable NF-κB and mitogen-activated protein kinase (MAPK) family members, resulted in striking differences cytokine chemokine gene transcription, suggesting signaling is not equivalent. A agonist specifically promoted the production Th1-inducing interleukin (IL) 12 p70 interferon-γ inducible (IP)-10, which also associated Th1 responses. In contrast, stimulation failed induce IL-12 (IP)-10 but release inhibitory p40 homodimer, producing conditions are predicted favor Th2 development. preferential induction IL-8 p19/IL-23. Involvement phosphatidylinositol 3-kinase p38 MAPK TLR-mediated several messages was demonstrated using specific inhibitors. Thus, TLRs can translate information regarding nature pathogens into cytokines chemokines produced therefore may contribute polarization acquired immune response.