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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KIR2DS4del   Unknown Unpublished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, 8488]
Slower disease progression KIR3DS1 HLA-Bw4-80I Slower disease progression; Robust expansion during early infection; Inhibition in vitro viral replication [5961]
   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]
  1. 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]