| Literature DB >> 27332732 |
Duojiao Wu1, David E Sanin2, Bart Everts3, Qiongyu Chen4, Jing Qiu2, Michael D Buck2, Annette Patterson5, Amber M Smith4, Chih-Hao Chang4, Zhiping Liu6, Maxim N Artyomov4, Erika L Pearce2, Marina Cella4, Edward J Pearce7.
Abstract
Greater understanding of the complex host responses induced by type 1 interferon (IFN) cytokines could allow new therapeutic approaches for diseases in which these cytokines are implicated. We found that in response to the Toll-like receptor-9 agonist CpGA, plasmacytoid dendritic cells (pDC) produced type 1 IFNs, which, through an autocrine type 1 IFN receptor-dependent pathway, induced changes in cellular metabolism characterized by increased fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS). Direct inhibition of FAO and of pathways that support this process, such as fatty acid synthesis, prevented full pDC activation. Type 1 IFNs also induced increased FAO and OXPHOS in non-hematopoietic cells and were found to be responsible for increased FAO and OXPHOS in virus-infected cells. Increased FAO and OXPHOS in response to type 1 IFNs was regulated by PPARα. Our findings reveal FAO, OXPHOS and PPARα as potential targets to therapeutically modulate downstream effects of type 1 IFNs.Entities:
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Year: 2016 PMID： 27332732 PMCID： PMC5695232 DOI： 10.1016/j.immuni.2016.06.006
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745