3a). More specifically, the frequency of NKG2A+CD3+CD8− cells in the HAART group was lower than that of the AIDS group (P < 0.05), while there was no significant

difference in NKG2A expression between the HAART group and the normal control group. The same potentially HAART-induced reverse was observed for NKG2A+NKG2D−CD3+CD8− cells (Fig. 3b). HAART treatment decreased the frequency of NKG2D on CD3+CD8− cells compared with AIDS group (P < 0.01) (Fig. 3c). The expression of NKG2D+NKG2A− on CD3+CD8− cells in HAART group were lower than AIDS group (P < 0.05, Fig. 3d), so did the expression of NKG2D+KIR3DL1− (P < 0.001, selleck kinase inhibitor Fig.3e). We analyzed the relationships among NKR expression, CD4+ T cell counts and HIV viral loads. For CD8+ T cells, the percentages of NKG2A+CD8+ T and NKG2A+NKG2D−CD8+ T cells were negatively correlated with CD4+ T cell counts (r =−0.463, P < 0.01; r=−0.499, P < 0.01, respectively, Fig. 4a,b). In contrast, the percentage of NKG2D+NKG2A−CD8+ MI-503 cell line T cells was positively correlated with CD4+ T cell counts (r = 0.494, P < 0.01, Fig. 4c). No correlations between CD8+ T cell NKR expression and viral loads were observed. However, the frequency of NKG2A+NKG2D−CD8+ T cells tended to positively correlate with viral loads, while the prevalence of NKG2D+NKG2A−CD8+ T cells tended to negatively correlate with viral loads (Fig.

4d,e). Regarding CD3+CD8− cells, we found that CD3+CD8−

cell expression of NKG2D exhibited a strong positive correlation with HIV viral load (r= 0.455, P < 0.05) (Fig. 5a). Similarly, the percentages of NKG2D+NKG2A−CD3+CD8− (Fig. 5b) and NKG2D+KIR3DL1−CD3+CD8− cells (Fig. 5c) were positively correlated with viral loads (r= 0.527, P < 0.01, and r= 0.438, P < 0.05, respectively). NKG2D+NKG2A− and NKG2D+KIR3DL1− expression on CD3+CD8− cells were negatively correlated with CD4+ T cell counts (r=−0.397, P < Ribonuclease T1 0.05, and r=−0.476, P < 0.05, respectively, Fig. 5d,e). Finally, the frequency of NKG2D+NKG2A+ on CD3+CD8− cells were negatively correlated with CD4+ T cell counts (r=−0.446, P < 0.01, Fig. 5f). NKRs are important regulators of T cell function. As impaired T cell function has been reported in chronic HIV infection, (23) we analyzed whether dysregulated expression of NKRs on lymphocyte subpopulations was involved in HIV infection. We observed no significant difference in the individual expression of NKG2D on CD8+ T cells among any of the four groups studied. However, the frequency of NKG2D+NKG2A−CD8+ T cells decreased during HIV infection in comparison to HIV-negative controls. The reduction of NKG2D+NKG2A−CD8+ T cells in patients with HIV infection could decrease the ability of cytotoxic T lymphocytes to recognize and lyse infected cells, resulting in an impaired immune response.