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-Related Apoptosis-Inducing Ligand in the Enhanced Cytotoxicity of IFN-
-Stimulated Human Dendritic Cells to Tumor Cells1
Department of Immunology, Second Military Medical University, Shanghei, People’s Republic of China
TNF-
-related apoptosis-inducing ligand (TRAIL) is characterized
by its preferential induction of apoptosis of tumor cells but not
normal cells. Dendritic cells (DCs), besides their role as APCs, now
have been demonstrated to exert cytotoxicity or cytostasis on some
tumor cells. Here, we report that both human CD34+ stem
cell-derived DCs (CD34DCs) and human CD14+ monocyte-derived
DCs (MoDCs) express TRAIL and exhibit cytotoxicity to some types of
tumor cells partially through TRAIL. Moderate expression of TRAIL
appeared on CD34DCs from the 8th day of culture and was also seen on
freshly isolated monocytes. The level of TRAIL expression remained
constant until DC maturation. TRAIL expression on immature CD34DCs or
MoDCs was greatly up-regulated after IFN-
stimulation. Moreover,
IFN- could strikingly enhance the ability of CD34DCs or MoDCs to
kill TRAIL-sensitive tumor cells, but LPS did not have such an effect.
The up-regulation of TRAIL on IFN--stimulated DCs partially
contributed to the increased cytotoxicity of DCs. Pretreatment of
TRAIL-sensitive tumor cells with caspase-3 inhibitor could
significantly increase their resistance to the cytotoxicity of
IFN--stimulated DCs. In contrast, NF-
B inhibitor could
significantly increase the sensitivity of tumor cells to the killing by
nonstimulated or LPS-stimulated DCs. Our studies demonstrate that
IFN--stimulated DCs are functionally cytotoxic. Thus, an innate
mechanism of DC-mediated antitumor immunity might exist in vivo in
which DCs act as effectors to directly kill tumor cells partially via
TRAIL. Subsequently, DCs act as APCs involved in the uptake,
processing, and presentation of apoptotic tumor Ags to cross-prime
CD8+ CTL cells.
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