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Mediates a Novel Antiviral Activity Through Dynamic Modulation of TRAIL and TRAIL Receptor Expression
Departments of
*
Molecular Immunology,
Molecular Biology, and
Bioinformatics, Immunex Corporation, Seattle, WA 98101
TNF-related apoptosis-inducing ligand (TRAIL) is able to kill many
transformed cells of diverse tissue types. We show that TRAIL is
inducible by IFN-
, by TNF-
, and by infection with human CMV, and
has potent antiviral activity in vitro. CMV infection and IFN- also
reciprocally modulate TRAIL receptor (TRAIL-R) expression. CMV
infection increased the expression of TRAIL-R1 and -R2, whereas IFN-
down-regulated the expression of TRAIL-Rs on uninfected fibroblasts.
Moreover, IFN- significantly decreased the basal level of NF-
B
activation, a known survival factor that inhibits apoptosis. Thus,
TRAIL selectively kills virus-infected cells while leaving uninfected
cells intact, and IFN- 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.
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