MULT1plying cancer immunity

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Science  03 Apr 2015:
Vol. 348, Issue 6230, pp. 45-46
DOI: 10.1126/science.aaa9842

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Immunotherapy of cancer, based on natural killer (NK) cells, is an emerging field (1). Activation of these innate lymphocytes depends on signals emanating from receptors that recognize transformed cells. The extent and spectrum of receptor engagement by cognate ligands that tumors bear determines the outcome of NK cell responses, including direct cellular killing (through the release of cytolytic granules) and communication with other immune cells (through secreted cytokines). One potent activating NK cell receptor involved in the destruction of ligand-expressing transformed cells is natural-killer group 2, member D (NKG2D). Recently, however, an immunosuppressive role was attributed to persistently engaged NKG2D. On page 136 of this issue, Deng et al. (2) report that, contrary to expectations, release of a particular NKG2D ligand by tumor cells results in NK cell activation and enhanced tumor rejection in a mouse model. This remarkable result may open new treatment options for cancer patients.