Table 3 Chemokine receptor engineering to improve NK cell migration

From: Development of NK cell-based cancer immunotherapies through receptor engineering

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]