Figure 1 - Model of KIR3DL1 and KIR3DS1 interactions with HLA-B Bw4-80I expressed on HIV-uninfected and HIV-infected cells.

(a) When KIR3DL1 is highly expressed on NK cells, the interaction with HLA-B Bw4-80I molecules on uninfected cells expressing self peptides results in a strong inhibitory signal to NK activity. HIV-1 infection leads to downregulation of HLA-B Bw4-80I on infected cells and presentation of viral or stress peptides, resulting in loss of the strong NK cell inhibition mediated by high expression of KIR3DL1 and in subsequent target cell lysis. (b) KIR3DS1 expressed on NK cells does not bind to HLA-B Bw4-80I presenting normal HLA-B Bw4-80I displaying self peptides but may recognize viral or stress peptides presented by HLA-B Bw4-80I on infected cells, resulting in NK cell activation and target cell lysis.

Kim Caesar