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Division of Rheumatology/Howard Hughes Medical Institute, Washington University School of Medicine and Barnes-Jewish Hospital, St. Louis, MO 63110
The activation of NK cells is mediated through specific
interactions between activation receptors and their respective ligands.
Little is known, however, about whether costimulation, which has been
well characterized for T cell activation, occurs in NK cells. To study
the function of NKG2D, a potential NK costimulatory receptor, we have
generated two novel hamster mAbs that recognize mouse NKG2D. FACS
analyses demonstrate that mouse NKG2D is expressed on all C57BL/6
IL-2-activated NK (lymphokine-activated killer (LAK)) cells, all
splenic and liver NK cells, and 
50% of splenic NKT cells.
Consistent with limited polymorphism of NKG2D, its sequence is highly
conserved, and the anti-NKG2D mAbs react with NK cells from a large
number of different mouse strains. In chromium release assays, we show
that stimulation of NK cells with anti-NKG2D mAb can redirect
lysis. Also, enhanced lysis of transfected tumor targets expressing
NKG2D ligand could be inhibited by addition of anti-NKG2D mAb.
Interestingly, stimulation of LAK cells via NKG2D alone does not lead
to cytokine release. However, stimulation of LAK via both an NK
activation receptor (e.g., CD16, NK1.1, or Ly-49D) and NKG2D leads to
augmentation of cytokine release compared with stimulation through the
activation receptor alone. These results demonstrate that NKG2D has the
ability to costimulate multiple NK activation
receptors.
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