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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.

Interferon contributes to photosensitivity at least in part by causing Langerhans cell ADAM17 dysfunction, raising the possibility that anifrolumab ameliorates lupus skin disease in part by restoring Langerhans cell function.

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.

By joining the Skp1-Cul1-Rbx1 SCF complex, Fbxo21 interacts with ASK1 and mediates Lys29-linkage of ASK1, leading to type I IFN production.

The induction of ISG15 during bacterial infection can be independent of Type I Interferons and leads to an increase in the secretion of cytokines known to be critical for bacterial clearance.

Computational analyses and biochemical measurements redefine the mechanisms by which pyrin-only-proteins specifically target and regulate the assembly of inflammasomes.

We are writing to comment on the study by Meyer et al., 2016 on disease-ameliorating autoantibodies.

Overlapping action of type I, II, and III interferons maintains microbiome homeostasis, prevents IL-17-driven myeloproliferative disease, and protects against inflammatory bowel disease.

In a study of a herpes simplex virus (HSV) vaccine, the combination of sex and prior exposure to the virus resulted in HSV naive women mounting a prominent type I interferon response associated with reduced neutralizing titers to HSV.

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.