Abstract
Abstract Plasmacytoid dendritic cells (pDCs) are specialized for the secretion of type I interferons (IFN-I) and thus are considered mediators of antiviral responses. pDCs selectively express endosomal Toll-like receptor (TLR) 7 and TLR9 and the ligation of TLR7/9 leads to rapid cellular activation. Recently, we found that stimulation of pDCs with the TLR9 agonist CpG resulted in a marked increase in mitochondrial oxygen consumption rates (OCR) dependent on increased fatty acid oxidation (FAO). FAO is essential for full activation of CpG-stimulated pDCs because etomoxir or carnitine palmitoyltransferase 1A shRNA (short-hairpin RNA) severely attenuated IFN-alpha production by these cells. Using RNA-seq, we identified the expression of many interferon-stimulated genes (ISG) in CpG-stimulated pDCs, amongst which were genes encoding FAO pathway components. We found that IFNAR -/- pDCs failed to increase mitochondrial OCR in response to TLR9 agonists. Taken together, our data indicate that IFN-alpha-induces FAO which is essential for full pDC activation in response to CpG.
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