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- W2002258448 abstract "The phenomenon of endotoxin sensitization by virus infection is well documented but not yet well understood. Infection by virtually any viral agent will quickly induce expression of type I interferons (IFN-alpha/beta), and type II IFN-gamma production will follow as NK cells and T cells are activated. It has been well established that type II IFN pretreatment can intensify the effects of endotoxin. We have recently demonstrated that type I IFN induction by lymphocytic choriomeningitis virus (LCMV) infection dramatically increases TNF-alpha production following LPS treatment, and that this sensitization by type I IFN is STAT1 dependent. Taken together these data suggest that the STAT1-mediated, MyD88-independent, arm of the LPS signaling pathway plays an important role in endotoxin toxicity, and that this pathway mediates a major component of virus-enhanced LPS sensitization." @default.
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- W2002258448 date "2003-10-01" @default.
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- W2002258448 title "The role of STAT1 in viral sensitization to LPS" @default.
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- W2002258448 doi "https://doi.org/10.1179/096805103225002575" @default.
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