Figure 5
Figure 5. Interfering with the interaction between NKG2D and its ligands on HIV-infected T cells decreases NK-cell killing of the infected cells. (A,B,D) CD4−/HIV-1 p24 Ag+ HIV-1SF162– or (C) HIV-1SF128A–infected primary T cells were exposed to autologous NK cells treated in the absence (▓) or presence (□) of anti-NKG2D blocking monoclonal antibodies or anti-NKp46 blocking monoclonal antibodies (panel D, ▒) in a 4-hour cytotoxicity assay (*, P < .05; t test). Error bars represent standard deviation of the mean. Panels A,B, and D are 3 separate donors; panels C and D are from the same donor.

Interfering with the interaction between NKG2D and its ligands on HIV-infected T cells decreases NK-cell killing of the infected cells. (A,B,D) CD4/HIV-1 p24 Ag+ HIV-1SF162– or (C) HIV-1SF128A–infected primary T cells were exposed to autologous NK cells treated in the absence (▓) or presence (□) of anti-NKG2D blocking monoclonal antibodies or anti-NKp46 blocking monoclonal antibodies (panel D, ▒) in a 4-hour cytotoxicity assay (*, P < .05; t test). Error bars represent standard deviation of the mean. Panels A,B, and D are 3 separate donors; panels C and D are from the same donor.

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