| First Author | Wu D | Year | 2016 |
| Journal | Immunity | Volume | 44 |
| Issue | 6 | Pages | 1325-36 |
| PubMed ID | 27332732 | Mgi Jnum | J:259239 |
| Mgi Id | MGI:6141232 | Doi | 10.1016/j.immuni.2016.06.006 |
| Citation | Wu D, et al. (2016) Type 1 Interferons Induce Changes in Core Metabolism that Are Critical for Immune Function. Immunity 44(6):1325-36 |
| abstractText | 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 PPARalpha. Our findings reveal FAO, OXPHOS and PPARalpha as potential targets to therapeutically modulate downstream effects of type 1 IFNs. |
