Topic: IFNAR1

We have recently established Rnaset2-/- mice as a model system to improve the pathophysiological understanding of infantile-onset RNaseT2-deficient leukoencephalopathies and type I interferonopathies. Rnaset2-/- mice were viable and healthy at birth, but displayed upregulation of type I interferon-stimulated genes in all organs examined. At 20 weeks of age, RNaseT2-deficient animals developed IFNAR1-dependent neuroinflammation, characterized primarily by the presence of CD8 T cells and inflammatory monocytes. Single nuclei transcriptome analyses revealed homeostatic dysfunction in glial cells

Individuals with autism spectrum disorder (ASD; autism) are more susceptible to inflammatory disorders and gastrointestinal dysfunction, but the cause is unknown. We investigated gut permeability and the impact of acute inflammatory insult on gut function and behaviour in Nlgn3R451C mice expressing an autism-associated mutation in Neuroligin-3. Ex vivo intestinal permeability was assessed by measuring the passage of FITC across the mucosa from the lumen. To compare impacts of modulating the nervous system with immune pathway disruption, we bred Nlgn3R451C mice with mice lacking the interferon