Table 3.

Chemokine receptor engineering to improve NK cell migration

Receptor	Target	NK sources	Modification techniques	Target disease	Outcomes	Ref
CXCR1	IL-8	PB	mRNA electroporation	Ovarian cancer	Greater chemiotaxis in vivo Increased tumor control	[123]
CXCR2	CXCL5	PB	Retroviral vector	Renal cell carcinoma	Greater chemiotaxis in vitro Increase target cell killing and adhesion in vitro	[120]
CXCR2	CXCL1-3 and CXCL5-8	NK92	CRISPR-Cas9	Human Colon Cancer	Greater chemiotaxis in vivo into tumor sites Stronger cell-killing and proliferation activity Tumor reduction Increased survival	[122]
CCR2B and CCR4	CCL22 or CCL2	NK-92 and PB	Lentiviral vector	None	Greater chemiotaxis in vitro	[130]
CXCR4	CXCL12 and SDF-1α	YTS	Lentiviral vector	Glioblastoma	Greater chemiotaxis in vitro and in vivo Tumor reduction/clearance Increased survival	[68]
CXCR4	SDF-1α	PB	Lentiviral vector	None	Greater chemiotaxis in vitro	[126]
CXCR4R334X	SDF-1α	PB	mRNA transfection	None	Greater chemotaxis in vitro Increased the bone marrow homing	[125]
CXCR4 and CCR7	CXCL12 and CCL21	NK92	Lentiviral vector	Colorectal cancers	Tumor reduction Increased survival	[127]
CCR5	CCL5	PB	Lentiviral vector	Human Colon Cancer	Greater chemiotaxis in vitro and in vivo	[132]
CCR7	CCL19 and CCL21	PB	Trogocytosis	None	Greater chemotaxis in vitro Increased the lymph node homing	[129]
CCR7	CCL19 and CCL21	NK-92	DNA transfection	B-cell lymphoma	Greater chemiotaxis in vitro and in vivo Increased tumor control Increased survival	[128]
CCR7	CCL19	PB	mRNA electroporation	None	Greater chemiotaxis in vitro	[109]