The role of NK cells in HIV-1 protection: autologous, allogeneic or both?

Hens, Jef; Jennes, Wim; Kestens, Luc

doi:10.1186/s12981-016-0099-6

AIDS Research and Therapy

Table 1 KIR and HLA genotypes related to HIV-1 outcome

From: The role of NK cells in HIV-1 protection: autologous, allogeneic or both?

HIV-1 outcome	Receptor/ligand		Mechanism	Ref
HIV-1 resistance	KIR3DS1/S1	HLA-Bw4	No/less inhibition and increased activation, promoting faster NK cell activation	[85, 86]
	KIR3DS1/x	HLA-Bw4	No/less inhibition and increased activation, promoting faster NK cell activation	[87]
	KIR3DS1/L1		Higher activating ratio, stronger NK cell response	[84]
	KIR3DL1*h	HLA-B*57	“Amplified” education, resulting in stronger NK cell response in absence of ligand	[72]
	KIR3DL1	Bw4	Educated KIR3DL1+ NK cells had increased anti-HIV-1 ADCC mediated cytotoxicity against allogeneic target cells	[76]
	KIR3DL1	HLA-Bw6/Bw6	Absence/lowering of inhibitory threshold, promoting faster NK cell activation	[88]
	KIR2DL2/3	HLA-C2/C2	Absence/lowering of inhibitory threshold	[88]
	KIR2DS4del		Unknown	Unpublished
	KIR2DL1	HLA-C2	Absence of HLA-C2 expression by allogeneic target cells induces cytotoxicity based on KIR/HLA mismatch	[6]
	Haplotype B/x		Multiple aKIRs inducing stronger response	[6, 84–88]
Slower disease progression	KIR3DS1	HLA-Bw4-80I	Slower disease progression; Robust expansion during early infection; Inhibition in vitro viral replication	[59–61]
			Increase of copy numbers is associated with inhibition of viral replication	[62]
			In vitro production of viral inhibiting chemokines (CCL3-5), preventing HIV-1 entry	[123]
	KIR3DS1	HLA-B*57/58	Lower CD38-expression, increased degranulation and IFN-γ production	[64]
	KIR3DS1		Associated with higher CD4+ T-cell counts	[63]
	KIR3DL1/S1	HLA-Bw4	KIR3DL1-dose dependent-licensed NK cells exert cytotoxicity via KIR3DS1-mediated activation	[66]
	KIR3DL1	HLA-Bw4	Increased polyfunctionality by KIR3DL1 licensed NK cells	[65]
			Educated KIR3DL1+ NK cells had increased anti-HIV-1 ADCC mediated activation	[75]
	KIR3DL1*h	HLA-Bw4-80I	Delayed progression to AIDS, increased degranulation, TNF and IFN-γ production	[66, 67]
	KIR3DL1*h	HLA-B*57	“Amplified” education, resulting in strong NK cell response, increased NK cell trifunctionality	[66, 68, 69]
			In vitro production of viral inhibiting chemokines (CCL3-5), preventing HIV-1 entry	[123]
	KIR3DL1*004	HLA-Bw4	Absence/lowering of inhibitory threshold, because of intracellular expression of KIR3DL1	[66]
	KIR2DL3	HLA-C1	Lower viral load and higher CD4 count associated with HIV-1 specific NK cell responses	[73]
	KIR2DL4		CD4+ T-cell preservation, higher copy number resulting in increased IFN-γ production in SIV-infection	[124]
Rapid disease progression	KIR3DS1	HLA-Bw4-80I	Rapid progression, no education of KIR3DS1 expressing NK cells	[80]
	KIR3DS1(/S1)		Rapid progression, robust immune activation accelerating disease progression	[59, 80]
	KIR2DS2/3		Rapid progression, robust immune activation accelerating disease progression	[80]
	KIR2DS4*001		High viral load and accelerated HIV-1 transmission, immune activation accelerating disease progression	[82]
	KIR2DL2/3	HLA-C1	Higher viral load and increased mortality	[83]
	Haplotype B/x		Rapid progression, robust immune activation accelerating disease progression	[80, 81]

Summarization of the KIR, HLA or KIR-HLA haplo-/genotypes associated with HIV-1 resistance and disease progression towards AIDS. HLA class I genotypes associated with altered HIV-1 outcome are not included as its function is not solely relevant for NK cell responses but also for CD8⁺ T cell responses. Additional data in Table 1 obtained from [123] and [124]

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ISSN: 1742-6405

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