Murine Mast Cells That Are Deficient in IFNAR-Signaling Respond to Viral Infection by Producing a Large Amount of Inflammatory Cytokines a Low Level of Reactive Oxygen Species and a High Rate of Cell Death.
Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b(+)Ly-6C(+) monocytes.
Interferon Type I Regulates Inflammasome Activation and High Mobility Group Box 1 Translocation in Hepatocytes During Ehrlichia-Induced Acute Liver Injury.
Type I interferons are essential while type II interferon is dispensable for protection against St. Louis encephalitis virus infection in the mouse brain.
Type I Interferon alpha/beta Receptor-Mediated Signaling Negatively Regulates Antiviral Cytokine Responses in Murine Bone-Marrow-Derived Mast Cells and Protects the Cells from Virus-Induced Cell Death.
The authors identified hepatocyte-intrinsic IFNAR1 signaling as a key regulator of circulating levels of arginine and ornithine to fine-tune adaptive immunity.
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