Derepression of transcripts from hypomethylated pericentromeric repeats triggers an innate immune response in an animal model of Immunodeficency, Centromere and Facial anomalies (ICF) syndrome.

Neutrophil-dependent innate immune responses to the human pathogen, methicillin-resistant Staphylococcus aureus, are modulated by an interplay between interleukin-21 and type 1 interferons.

Complex I of the mitochondrial respiratory chain is necessary for interferon gamma-mediated responses in antigen-presenting cells and is required for CD4+ T cell activation.

Def6 functions as a novel immunoregulator in bone cells via endogenous type-I interferon response to regulate bone remodeling.

The enteric bacterial microbiota stimulates a highly localized interferon-lambda signal within the intestinal epithelium that protects against murine rotavirus infection.

MiRNA-mediated suppression of MAVS expression in embryonic stem cells is necessary to inactivate the type I interferon response.

Knocking out Folliculin (FLCN) in human renal epithelial cells activates STAT1/2-mediated gene expression, independent of interferon, uncovering a tissue-specific process potentially relevant in the cancer syndrome Birt-Hogg-Dubé (BHD).

Hyperactive interferon signaling is a hallmark of trisomy 21 and may contribute to many of the comorbidities associated with Down syndrome.

In vivo study of arbovirus infections reveals the dominant role of pDC IRF7-signaling in directing both type I and II IFN responses, and leading to viral control.

An epigenomic analysis in mouse macrophages reveals that a highly abundant transposable element exhibits activity as an immune inducible regulatory element.