Aicardi–Goutières syndrome and the type I interferonopathies

By Y. Crow, N. Manel. Nature reviews. Immunology, 2015

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Shared and Distinct Functions of Type I and Type III Interferons (2019, neutral): “Women with dysregulated type I IFN signaling (sustained IFN production or impaired receptor downregulation) exhibit poor pregnancy outcomes including pre-eclampsia as well as neurodevelopmental defects similar to those induced by congenital infection, altogether consistent with a role for dysregulat”
Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence (2017, neutral): “Genetic defects that compromise endogenous DNA metabolism or instances that trigger massive, synchronized accumulation of dead cells represent examples of this phenomenon 26 27 28, 29 30.”
R-loops as cellular regulators and genomic threats (2019, background): “It is attributed to mutations in nucleic acid-degrading enzymes, including TREX1, SAMHD1 and RNase H2, which cause endogenous nucleic acids to accumulate in the cytoplasm of cells and ultimately activate the cGAS-STING pathway and interferon responses (Crow and Manel, 2015).”
Mitochondrial DNA in inflammation and immunity (2020, neutral): “In humans, the systemic inflammatory disease Aicardi– Goutières syndrome (AGS) is characterised by mutations in a number of different genes involved in DNA sensing [88].”