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• W2782358550 abstract "The autoimmune disorder Aicardi-Goutières syndrome (AGS) is characterized by a constitutive type I interferon response. SAMHD1 possesses both dNTPase and RNase activities and mutations in SAMHD1 cause AGS; however, how SAMHD1-deficiency causes the type I interferon response in patients with AGS remains unknown. Here, we show that endogenous RNA substrates accumulated in the absence of SAMHD1 act as a major immunogenic source for the type I interferon response. Reconstitution of SAMHD1-negative human cells with wild-type but not RNase-defective SAMHD1 abolishes spontaneous type I interferon induction. We further identify that the PI3K/AKT/IRF3 signaling pathway is essential for the type I interferon response in SAMHD1-deficient human monocytic cells. Treatment of PI3K or AKT inhibitors dramatically reduces the type I interferon signatures in SAMHD1-deficient cells. Moreover, SAMHD1/AKT1 double knockout relieves the type I interferon signatures to the levels observed for wild-type cells. Identification of AGS-related RNA sensing pathway provides critical insights into the molecular pathogenesis of the type I interferonopathies such as AGS and overlapping autoimmune disorders." @default.
• W2782358550 created "2018-01-12" @default.
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• W2782358550 date "2018-01-08" @default.
• W2782358550 modified "2023-10-12" @default.
• W2782358550 title "A central role for PI3K-AKT signaling pathway in linking SAMHD1-deficiency to the type I interferon signature" @default.
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• W2782358550 doi "https://doi.org/10.1038/s41598-017-18308-8" @default.
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• W2782358550 hasPublicationYear "2018" @default.
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