Triplication of the Ifnr locus drives increased IFNR protein expression and an aberrant anti-viral response in a mouse model of Down syndrome.

Representative flow cytometry histograms or psuedocolor density plots of white blood cells from the Dp16 mouse model of Down syndrome, Dp16 corrected for Ifnr dosage (Dp162xIfnrs), and wildtype controls (WT). Peripheral blood was collected from the submandibular vein of mice 17-25 weeks of age into tubes of lithium heparin, then stained and analysed as previously described with minor alterations specified in the methods section.