The Journal of Immunology · 2012 · 82 citations · 30 references
Life SciencesCell BiologyImmunologyCell SignalingInflammationInnate ImmunityCytokine BiologyCytokine SignalingDendritic Cell BiologyInflammatory Cell ResponsesInflammatory SignalingT Cell ActivationDendritic Cell Cytokine ProductionDendritic Cell Cytokine SignalingDendritic Cell Inflammatory ResponsesDendritic Cell SignalingDendritic Cell-driven T Cell PrimingDendritic Cell-mediated T Cell ActivationDendritic Cell-t Cell InteractionTh17 Responses
LPS-activated dendritic cells (DCs) are thought to follow a set program in which they secrete inflammatory cytokines (such as IL-12) and then become refractory to further stimulation (i.e., "exhausted"). In this study, we show that mouse DCs do indeed lose their responsiveness to LPS, but nevertheless remain perfectly capable of making inflammatory cytokines in response to signals from activated T cells and to CD40-ligand and soluble T cell-derived signals. Furthermore, far from being rigidly programmed by the original activating stimulus, the DCs retained sufficient plasticity to respond differentially to interactions with Th0, Th1, Th2, and Th17 T cells. These data suggest that LPS activation does not exhaust DCs but rather primes them for subsequent signals from T cells.
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