Hematological Malignancies Escape from NK Cell Innate Immune Surveillance: Mechanisms and Therapeutic Implications

Table 1

Mechanisms of escape, receptor, and ligand involved and type of hematological malignancy.

Mechanisms of escape	Receptor in NK cells	Ligand in tumor cells	Hematological malignancy type	References
NK-cell quantitative deficiency			MDS	[5, 11]
Increased expression of inhibitory receptors		Upregulation of HLA class I	AML	[12–14]
			CLL; LAL	[14, 15]; [14]
			MM	[16]
			Lymphoma	[17]
Decreased activation by decreased expression of activating receptor or their ligands	NKp30		AML	[8, 18–20]
	NKp46NKG2D		CLL	[21]
		NCR-ligand	AML
			LGL	[8]
		sMICA and sMICB	CLL	[22]
			CML	[23]
			MM
			ALL	[24]
	DNAM1	NKG2D on tumor cells	CMML	[25]
				[26]
	CD94/NKG2C		AML
				[27]
	2B4/CD244		AML
				[27]
	CD16		AML
			MM	[27]
			MM	[28, 29]
				[28, 29]
Impaired NK cell differentiation signaling			CML	[30]
			PV	Personal data
Impaired cytokine production	Elevated TNF		MDS	[31]
	Elevated PDGF		MPS	[32]
	Elevated TGFb			[33]
	Decreased IL1		AML	[34]
	IL2 and IFN𝛾		ALL	[34]

Abbreviations: MDS: myelodysplastic syndrome; MPS: myeloproliferative syndrome; ALL: acute lymphoid leukemia; AML: acute myeloid leukemia; CML: chronic myeloid leukemia; MM: multiple myeloma; CMML: myelomonocytic leukemia; LGL: large granular lymphoma; PV: polycythemia vera; sMICA: stress-induced molecule HLA class-I chain-related A; IL: interleukin; IFN𝛾: interferon-gamma.