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10.1016/j.immuni.2016.06.006

http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.06.006
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C5695232!5695232!27332732
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suck abstract from ncbi


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pmid27332732      Immunity 2016 ; 44 (6): 1325-36
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  • Type 1 interferons induce changes in core metabolism that are critical for immune function #MMPMID27332732
  • Wu D; Sanin DE; Everts B; Chen Q; Qiu J; Buck MD; Patterson A; Smith AM; Chang CH; Liu Z; Artyomov MN; Pearce EL; Cella M; Pearce EJ
  • Immunity 2016[Jun]; 44 (6): 1325-36 PMID27332732show ga
  • Greater understanding of the complex host responses induced by type 1 Interferon (IFNs) 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 PPAR?. Our findings reveal FAO, OXPHOS and PPAR? as potential targets to therapeutically modulate downstream effects of type 1 IFNs.
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