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Regulation of translation is required for dendritic cell function and survival during activation
Correspondence to Philippe Pierre: pierre{at}ciml.univ-mrs.fr
In response to inflammatory stimulation, dendritic cells (DCs) have a remarkable pattern of differentiation (maturation) that exhibits specific mechanisms to control antigen processing and presentation. Here, we show that in response to lipopolysaccharides, protein synthesis is rapidly enhanced in DCs. This enhancement occurs via a PI3K-dependent signaling pathway and is key for DC activation. In addition, we show that later on, in a manner similar to viral or apoptotic stress, DC activation leads to the phosphorylation and proteolysis of important translation initiation factors, thus inhibiting cap-dependent translation. This inhibition correlates with major changes in the origin of the peptides presented by MHC class I and the ability of mature DCs to prevent cell death. Our observations have important implications in linking translation regulation with DC function and survival during the immune response.
Abbreviations used in this paper: CHX, cycloheximide; DALIS, dendritic cell aggresome-like induced structures; DC, dendritic cell; iDC, immature DC; IRES, internal ribosome entry site; LPS, lipopolysaccharide; mDC, maturing DC; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide-3-kinase; TRIF, Toll-IL-1 receptor domain-containing adaptor-inducing IFN-β.
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