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*
Research Center for Cell Transplantation,
Department of Pediatrics, and
Department of Hematology and Rheumatology, Tokai University, School of Medicine, Kanagawa, Japan; and
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California at San Diego Medical Center, San Diego, CA 92103
NK cells and dendritic cells (DCs) are both important in the innate
host defense. However, the role of DCs in NK cell-mediated cytotoxicity
is unclear. In this study, we designed two culture systems in which
human cord blood CD34+ cells from the same donor were
induced to generate NK cells and DCs, respectively. Coculture of the NK
cells with DCs resulted in significant enhancement of NK cell
cytotoxicity and IFN-
production. However, NK cell cytotoxicity and
IFN- production were not increased when NK cells and DCs were grown
together separated by a transwell membrane. Functional studies
demonstrated that 1) concanamycin A, a selective inhibitor of
perforin/granzyme B-based cytolysis, blocked DC-stimulated NK
cytotoxicity against K562 cells; and 2) neutralizing mAb against Fas
ligand (FasL) significantly reduced DC-stimulated NK cytotoxicity
against Fas-positive Jurkat cells. In addition, a marked increase of
FasL mRNA and FasL protein expression was observed in DC-stimulated NK
cells. The addition of neutralizing mAb against IL-18 and IL-12
significantly suppressed DC-stimulated NK cell cytotoxicity.
Neutralizing IFN- Ab almost completely inhibited NK cell
cytotoxicity against Jurkat cells. These observations suggest that DCs
enhance NK cell cytotoxicity by up-regulating both perforin/granzyme B-
and FasL/Fas-based pathways. Direct interaction between DCs and NK
cells is necessary for DC-mediated enhancement of NK cell cytotoxicity.
Furthermore, DC-derived IL-18 and IL-12 were involved in the
up-regulation of NK cell cytotoxicity, and endogenous IFN-
production plays an important role in Fas-mediated cytotoxicity.
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