Skip to main content
. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Exp Hematol. 2019 Jan 4;71:13–23. doi: 10.1016/j.exphem.2018.12.005

Figure 2. Regulation of NK cell activity.

Figure 2.

NK cells are a key meditator of anti-tumor and antiviral activity. (A) Normally, NK cell activity is balanced by engagement of activating and inhibitory receptors to prevent killing of normal (non-tumor and non-infected) cells. (B) Tumor cells may down-regulate expression of major histocompatibility complex (MHC) class I molecules to avoid T cell-mediated killing that requires MHC Class I expression. MHC class I molecules bind KIRs that mediate inhibitory signals for NK cells. Therefore, the loss of MHC class I on tumor cells can shift the balance towards activating receptors leading to secretion of granules containing granzymes and perforins to kill the tumor cells. (C) Another mechanism of action for NK cells is the recognition of specific antigens through the binding of CD16 with antigen-specific antibodies even if the overexpression of inhibitory ligands by tumor cells and the cleavage of CD16 on NK cells may inhibit their activation. (D) Overexpression of modified non-cleavable CD16 on hESC or hiPSC-derived NK cells can increase the activating signal to overcome the inhibitory signals from tumor cells. (E) CAR-expressing NK cells, such as those that can be derived from hESCs or hiPSCs can mediate anti-tumor activity by providing additional activating signals through the specific binding of the CARs to their antigens expressed on tumor cells.