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pubmed-article:10395688pubmed:abstractTextTNF-related apoptosis-inducing ligand (TRAIL) is able to kill many transformed cells of diverse tissue types. We show that TRAIL is inducible by IFN-gamma, by TNF-alpha, and by infection with human CMV, and has potent antiviral activity in vitro. CMV infection and IFN-gamma also reciprocally modulate TRAIL receptor (TRAIL-R) expression. CMV infection increased the expression of TRAIL-R1 and -R2, whereas IFN-gamma down-regulated the expression of TRAIL-Rs on uninfected fibroblasts. Moreover, IFN-gamma significantly decreased the basal level of NF-kappaB activation, a known survival factor that inhibits apoptosis. Thus, TRAIL selectively kills virus-infected cells while leaving uninfected cells intact, and IFN-gamma potentiates these effects by dynamic modulation of TRAIL and TRAIL-R expression and by sensitizing cells to apoptosis. The regulation of TRAIL and TRAIL-R expression may represent a general mechanism that contributes to the control of TRAIL-mediated apoptosis.lld:pubmed
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pubmed-article:10395688pubmed:articleTitleIFN-gamma mediates a novel antiviral activity through dynamic modulation of TRAIL and TRAIL receptor expression.lld:pubmed
pubmed-article:10395688pubmed:affiliationDepartment of Molecular Immunology, Immunex Corporation, Seattle, WA 98101, USA. sedger1@immunex.comlld:pubmed
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