Extracellular UDP and P2Y6 function as a danger signal to protect mice from vesicular stomatitis virus infection through an increase in IFN-β production.

Extracellular UDP and P2Y6 Function as a Danger Signal To Protect Mice from Vesicular Stomatitis Virus Infection through an Increase in IFN-b Production

hsp70-dependent antiviral immunity against cytopathic neuronal infection by vesicular stomatitis virus.

The major inducible 70-kDa heat shock protein (hsp70) protects against measles virus (MeV) neurovirulence in the mouse that is caused by a cell-associated noncytolytic neuronal infection. Protection is type I interferon (IFN) dependent, and we have established a novel axis of antiviral immunity in which hsp70 is released from virus-infected neurons to induce IFN-β in macrophages. The present wo...

Negative regulation of Nmi on virus-triggered type I IFN production by targeting IRF7.

Viral infection causes host cells to produce type I IFNs, which play a critical role in viral clearance. IFN regulatory factor (IRF) 7 is the master regulator of type I IFN-dependent immune responses. In this article, we report that N-Myc and STATs interactor (Nmi), a Sendai virus-inducible protein, interacted with IRF7 and inhibited virus-triggered type I IFN production. The overexpression of ...

Lithium attenuates IFN-β production and antiviral response via inhibition of TANK-binding kinase 1 kinase activity.

Lithium salt is a widely used glycogen synthase kinase-3β inhibitor and effective drug for the treatment of psychiatric diseases. However, the effects of lithium in innate immune responses, especially in cellular antiviral responses, are unknown. In this study, we show that lithium chloride attenuates LPS-, polyinosinic-polycytidylic acid-, and Sendai virus-induced IFN-β production and IFN regu...

Concomitant TLR/RLH signaling of radioresistant and radiosensitive cells is essential for protection against vesicular stomatitis virus infection.

Several studies indicated that TLR as well as retinoic acid-inducible gene I-like helicase (RLH) signaling contribute to vesicular stomatitis virus (VSV)-mediated triggering of type I IFN (IFN-I) responses. Nevertheless, TLR-deficient MyD88(-/-)Trif(-/-) mice and RLH-deficient caspase activation and recruitment domain adaptor inducing IFN-β (Cardif)(-/-) mice showed only marginally enhanced sus...