Topic: IFNAR

Type I interferons are most commonly associated with their essential role in the innate immune response. However, the actions of the type I interferon receptor are not limited to the scenario of infection. Previous work from our group revealed that type I interferon receptor signaling, specifically in a subtype of glia cells (astrocytes), critically modulates hippocampal synaptic plasticity and cognitive function in adult mice under physiological conditions. Since cytokines such as type I interferons are implicated in modulation of neurogenesis and brain development, in this work we started to

Type I interferon (IFN-I) is a pivotal cytokine of the innate immune response, playing a significant role in the pathophysiology of inflammation-induced damage in the central nervous system (CNS). Enhanced, constitutive IFN-I signaling is a defining feature of a number of Mendelian inborn errors of immunity, which are coined type I interferonopathies. However, understanding the pathophysiology of these disorders is hindered by the inability of numerous animal models to replicate the neurological phenotype essential for these diseases. Fortunately, we have recently generated and characterized t