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Kennedy Institute of Rheumatology, London, United Kingdom
NK cells recognize and kill tumor cells and normal cells, and these
play an important role in immune defense in cancer, infectious disease,
and autoimmunity. NK killing is regulated by positive or negative
signals derived from the interaction of surface receptors with ligands
on the target cells. However, the mechanisms controlling the
proliferation and maintenance of NK cells in normal human individuals
are less clearly defined. In this study, using an entirely autologous
system, we demonstrate that human peripheral blood
CD3-CD56+, killer cell-inhibitory
receptor (KIR)-expressing cells proliferate and expand in response to
LPS. These responses are enhanced in the presence of anti-IL-10
receptor-blocking Abs or on the removal of CD14+ cells from
the cultures. This enhancement is also reflected in substantial
increases in cytolytic activity and IFN-
production. The negative
effect of CD14+ cells may also be IL-10 mediated, IL-10
being lost from the culture supernatants of CD14-depleted PBMC and
rIL-10 reversing the effect of this depletion. On the other hand, mRNA
for the p35 and p40 subunits of IL-12 is still induced in CD14-depleted
cultures. The expansion of CD3-CD56+ cells was
also inhibited by CTLA4-Ig, indicating a role for CD80/86. B
lymphocytes were not required for the expansion of
CD3-CD56+ cells, whereas removal of MHC class
II+ cells from CD14-depleted cultures resulted in a
complete abrogation of these responses. Expansion of
CD3-CD56+ cells was reconstituted in MHC class
II-depleted cell cultures by adding back monocyte-derived dendritic
cells. These results indicate that the responses of
CD3-CD56+ NK cells to LPS may be driven by a
MHC class II+ B7+ CD14- peripheral
population, most likely blood dendritic cells.
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