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

Repression of type I interferons by SP140 is essential for resistance to Legionella pneumophila and Mycobacterium tuberculosis.

Type I IFN is a key determinant of pathogenic neutrophil activity and drives tissue pathology through modulation of IL-18 levels during genital HSV infection.

Cytomegaloviruses are recognized by distinct sensors depending on the infected cell type and together these sensors are essential for viral control and downstream immune responses.

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.

Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.

Selectively eliminating resident astrocytes in lumbar enlargement attenuated neuropathic pain associated with type I interferons (IFNs) signal activation in microglia.

CD169⁺ macrophages in the bone marrow of malaria-infected mice uptake infected red blood cells, and establish a functional interaction that is required to activate plasmacytoid dendritic cells to secrete type I interferon and leave the bone marrow.

The first lethal Junín virus challenge model in immunocompetent mice provides insight into New World mammarenavirus pathogenesis and will serve as a model for the development of much-needed therapeutic interventions.

Long studied in the context of the central nervous system, LRRK2 also functions in peripheral immunity by maintaining mitochondrial homeostasis in macrophages to regulate the type I interferon response.