Autoinflammation with enhanced type I interferon signaling due to DNASE2 mutations

In humans, microbial nucleic acid recognition serves as the major stimulus to an antiviral response, implying a requirement for cellular mechanisms to limit misrepresentation of self nucleic acids as non-self and the subsequent induction of type I interferon-mediated autoinflammation. This RNA-seq study was done on individuals with upregulated type I interferon signaling autoinflammatory disease.