RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.

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

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

CypA boosts RIG-I-mediated antiviral immune responses via enhancing K63-linked ubiquitination of RIG-I and inhibiting K48-linked ubiquitination of MAVS.

By inhibiting the activation of NF-κB, HIV-1 Vpu exerts much broader immunosuppressive effects than previously anticipated and may be an important determinant of chronic inflammation in HIV-1 infected individuals.

AXL enables the priming of the antiviral adaptive immune response by limiting the production of type I interferons in dendritic cells.

A gene expression data-informed model reveals that a small fraction of interferon-producing cells can effectively constrain early virus spread in epithelial tissue, elucidating connections between critical dynamics and infection heterogeneity.

In depth phenotyping from tissues and in vitro activation studies reveal antiviral function of MAIT cells- with particular emphasis on HIV infection.

Bats' uniquely robust innate antiviral immune defenses select for faster transmitting viruses likely to generate extreme virulence upon spillover to secondary hosts with immune systems divergent from those of bat.

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