Redox modification of STING represents a novel target for interferon regulation and control of herpesvirus replication.

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

The developmental transcription factor DUX4 interacts with STAT1 and broadly suppresses expression of IFNγ-stimulated genes.

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.

Host restriction factors that block cross-species transmission also play a role in limiting the replication of highly-adapted HIV-1 in IFN-stimulated cells.

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

The Mediator-associated kinases CDK8 and CDK19 help drive inflammatory responses to interferon, and it is discovered that kinase-dependent transcriptional responses manifest in part through splicing changes and lipid metabolites.

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

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

Overexpression of interferon-stimulated genes revealed a role for RARRES3 in restricting growth of Toxoplasma gondii by inducing early egress from human cells.