NK cells kill many types of tumor cells, especially cells that have reduced class I MHC expression and express ligands for NK cell activating receptors. In vitro, NK cells can kill virally infected cells and certain tumor cell lines, especially hematopoietic tumors. NK cells also respond to the absence of class I MHC molecules because the recognition of class I MHC molecules delivers inhibitory signals to NK cells (see Chapter 4, Fig. 4-6). As we shall see later, some tumors lose expression of class I MHC molecules, perhaps as a result of selection against class I MHC-expressing cells by CTLs. This loss of class I MHC molecules makes the tumors particularly good targets for NK cells. Some tumors also express MIC-A, MIC-B, and ULB, which are ligands for the NKG2D activating receptor on NK cells. In addition, NK cells can be targeted to IgG antibody-coated tumor cells by Fc receptors (FcyRIII or CD16). The tumoricidal capacity of NK cells is increased by cytokines, including interferon-y (IL-y), IL-15, and IL-12, and the anti-tumor effects of these cytokines are partly attributable to stimulation of NK cell activity. IL-2-activated NK cells, called lymphokine-activated killer (LAK) cells, are derived by culture of peripheral blood cells or tumor-infiltrating lymphocytes from tumor patients with high doses of IL-2. These cells are more potent killers of tumors than are unactivated NK cells. The use of LAK cells in adoptive immunotherapy for tumors is discussed later.
The importance of NK cells in tumor immunity in vivo is unclear. In some studies, T cell-deficient mice do not have a high incidence of spontaneous tumors, and this is attributed to the presence of normal numbers of NK cells that serve an immune surveillance function. A few patients have been described with deficiencies of NK cells and an increased incidence of EBV-associated lymphomas.
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