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Metabolic and Transcriptomic Effects of Mediator Kinase Inhibition on the Interferon Response in Down Syndrome

Down syndrome, also known as Trisomy 21, is a condition in humans resulting from full or partial triplication of chromosome 21. Affected individuals present with a constellation of symptoms that includes an increased risk of autoimmune disorders. Cells of patients with Down syndrome exhibit chronic, hyperactivated interferon (IFN) signaling, due in part to the presence of several interferon receptors on chromosome 21. Partial knockout of these receptors has been shown to increase cellular viability, indicating that treatments targeting the IFN response may ameliorate the comorbidities associated with Down syndrome.