Table 3.
Tumor cell survival mechanisms developed by tumor cells against NK cells.
| Tumor Cell Survival Mechanism | Effect (Reference) |
|---|---|
| Down-regulation of MICA/B and ULBP1/3 (NKG2D ligands) | NK cell inhibition [76,77] |
| Increased levels of soluble ULBP (NKG2D ligand) | NKG2D down-regulation, NK cell inhibition [78] |
| Increased levels of soluble B7-H6 (NKP30 ligand) | NKP30 down-regulation, NK cell inhibition [79] |
| Increased levels of soluble MICA/B (NKG2D ligand) | NK cell inhibition [80] |
| Release of pro-inflammatory molecules (MIF) | NKG2D down-regulation [81,82] |
| Transfer of NKG2D and NKP30 to tumor cells | NKG2D and NKP30 down-regulation in NK cells [69] |
| Up-regulation of inhibitory HLA-G | CAR-NK unresponsive to tumor cells [87] |
| PDL1 over-expression | PD-1 interaction with subsequent NK cell inhibition [90] |
| B7-H3 over-expression | NK cell inhibition [91] |
| TIM-3 over-expression | NK cell inhibition [93] |
NKG2D: also known as KLRK1 (killer cell lectin like receptor K1); NK: natural killer; NKP30: also known as NCR3 (natural cytotoxicity triggering receptor 3); CAR: chimeric antigen receptors; HLA: Human leukocyte antigen; MIF: migration inhibitory factor; PD-1: programmed cell death-1; PDL1: PD ligand 1; TIM-3: also known as PD-1.