Alteration of inhibitory and activating natural killer cell receptor expression on T cells in human immunodeficiency virus-infected Chinese.

T cell expression of NKRs can trigger or inhibit cell-mediated cytotoxicity. However, few studies on T lymphocyte NKR expression in HIV infection exist. Here, we examined the expression patterns of NKG2D, NKG2A, and KIR3DL1 on CD8⁺ and CD3⁺CD8⁻ cells by multicolor flow cytometry in groups of patients with HIV, AIDS or HAART-treated AIDS, as well as HIV-negative normal controls. Individual analysis of KIR3DL1 on CD3⁺ CD8⁺ or CD3⁺CD8⁻ cells revealed no significant differences among any of the groups (P > 0.05). In contrast, the percentage of NKG2A⁺NKG2D⁻CD8⁺ T cells was higher in the AIDS group than in the HIV-negative normal control group (P < 0.01). Meanwhile, the prevalence of NKG2D⁺ NKG2A⁻ CD8⁺ T cells was lower in the AIDS group than in HIV-negative normal controls (P < 0.001). Similar results were also observed for the percentage of NKG2A⁺ NKG2D⁻ on CD3⁺ CD8⁻ cells. However, in contrast to CD8⁺ T cells, the frequencies of NKG2D⁺ NKG2A⁻ on CD3⁺CD8⁻ cells were higher in AIDS and HIV patients than in HIV-negative normal controls (P < 0.01, P < 0.05, respectively). The percentage of NKG2A⁺NKG2⁻CD8⁺ T cells was negatively correlated with CD4⁺T cell counts (r=-0.499, P < 0.01), while the percentage of NKG2D⁺NKG2A⁻CD8⁺ T cells was positively correlated with CD4⁺ T cell counts (r= 0.494, P < 0.01). The percentage of NKG2D⁺NKG2A⁻CD3⁺CD8⁻ T cells was also positively correlated with viral load (r= 0.527, P < 0.01) and negatively correlated with CD4⁺ T cell counts (r=-0.397, P < 0.05). Finally, HAART treatment reversed the changes in NKR expression caused by HIV infection. These results indicate that the expression of NKRs on T cells may be correlated with HIV disease progression.