Expression of KLRG-1 on HIV-1–specific CD8⁺ T cells. (A) The expression levels of KLRG-1 on bulk CD8⁺ T cells varies, but it is not significantly different between chronic progressors and elite controllers. The horizontal lines at each variable indicate the mean. (B) A concatenation of samples from 14 HIV-1 chronic progressors and 11 HIV-1 elite controllers assessed for KLRG1 expression levels on tetramer-positive HIV-1–specific CD8⁺ T cells by flow cytometry. (C) Median fluorescent intensity of KLRG1 expression on HIV-1–specific tetramer-positive cells from 14 HIV-1 chronic progressors and 11 HIV-1 elite controllers. EBV- and CMV-specific cells were also analyzed for KLRG1 expression in both HIV-infected and -uninfected subjects. Antigen-specific CD8⁺ T cells from subjects with chronic-progressive disease had significantly higher levels of KLRG1 expression than subjects with controlled disease or cells specific for CMV or EBV, both mediators of latent viral infections. The horizontal lines at each variable indicate the mean. (D) The reduction in KLRG1 expression on epitope-specific CD8⁺ T cells after sequence evolution in the respective epitopes.³³  Primary flow data (left) and combined data for 8 subjects (right) for KLRG1 expression on epitope-specific CD8⁺ T cells before (wild-type) and after (escape) the selection of amino acid substitutions within the targeted epitopes are shown. The decrease of the KLRG-1 expression on tetramer-positive CD8⁺ T cells before and after the development of sequence variations within epitopes was statistically significant in frequency (P = .003 paired t test) and median fluorescent intensity (P = .002 paired t test).