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  Type 1 Interferons Induce Changes in Core Metabolism that Are Critical for Immune Function

Wu, D., Sanin, D. E., Everts, B., Chen, Q., Qiu, J., Buck, M. D., et al. (2016). Type 1 Interferons Induce Changes in Core Metabolism that Are Critical for Immune Function. Immunity, 44, 1325-1326. doi:org/10.1016/j.immuni.2016.06.006.

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Wu, Duojiao1, Author
Sanin, David E.1, Author
Everts, Bart1, Author
Chen, Qiongyu1, Author
Qiu, Jing1, Author
Buck, Michael D.1, Author
Patterson, Annette1, Author
Smith, Amber M.1, Author
Chang, Chih-Hao1, Author
Liu, Zhiping1, Author
Artyomov, Maxim N.2, Author
Pearce, Edward J.2, Author           
Cella, Marina1, Author
Pearce, Edward J.2, Author           
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1External Organizations, ou_persistent22              
2Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243648              

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 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.

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Language(s): eng - English
 Dates: 2016-06-21
 Publication Status: Issued
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 Rev. Type: Peer
 Identifiers: DOI: org/10.1016/j.immuni.2016.06.006
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Title: Immunity
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 44 Sequence Number: - Start / End Page: 1325 - 1326 Identifier: ISSN: 1074-7613
CoNE: https://pure.mpg.de/cone/journals/resource/954925604783