Abstract:
Abstract The stimulatory natural killer group 2 member
D (NKG2D) lymphocyte receptor, initially discovered and
expressed mostly on natural killer (NK) cells, T cells and
natural killer T cells, can promote tumor immune surveil-
lance. However, with increasing tumor grade, tumors
themselves express NKG2D to self-stimulate oncogenic
pathways. To confirm that cancer cells themselves express
NKG2D, we have now investigated the role of the tumoral
NKG2D in NK cell-mediated immune surveillance. Both
anti-NKG2D and shRNA to that down-regulated tumoral
NKG2D increased the number of cells in G1 phase and S
phase, increased the expression of cyclin E–CDK2 and
decreased P21. In addition, CD107a, IFN-c and TNF-a
increased when the cells were treated with anti-NKG2D
which suggests that blocking tumoral NKG2D could aug-
ment tumor surveillance of NK cells. Altogether, tumoral
NKG2D stimulates cell propaga