Figure 1
Figure 1. Up-regulated TRAIL surface expression on pDCs from HIV-1 viremic patients. (A) Percentage of various TRAIL+ cell types in subgroups of patients infected with HIV-1. Healthy HIV-1–seronegative persons (n = 13) served as control group. Data are given as mean percentages of TRAIL+ cells minus isotype controls ± SEM. (B) Individual VLs as well as (C) counts of CD4+ T cells were correlated with the percentage of TRAIL-expressing pDCs. (D) Percentages of TRAIL-expressing pDCs were determined in 6 patients infected with HIV-1 before cART initiation and after 8 to 12 weeks, when the VL had fallen below the limit of quantification (< 50 RNA copies/mL plasma) in each case. (E) Isolated pDCs from HIV-negative donors were stimulated with (1) AT-2 HIV-1 plus an isotype control, (2) AT-2 HIV-1 plus a neutralizing anti–IFN-α antibody, and (3) matched microvesicles (MVs) plus isotype control for 12 hours and subsequently FACS stained for surface TRAIL expression. Data are given as mean percentages of TRAIL-positive pDCs minus isotype controls ± SEM of 2 independent experiments. (F) Representative histogram plots of indicated patient groups show the surface expression of TRAIL on freshly isolated pDCs compared with an isotype control (open lines). (G) TRAIL-expressing pDCs in different viral diseases: viremic patients infected with HIV-1 (n = 20), viremic patients infected with HCV (n = 10), patients infected with primary VZV (n = 4), and healthy controls (n = 13). Data are given as mean percentages of TRAIL-positive pDCs minus isotype controls ± SEM.

Up-regulated TRAIL surface expression on pDCs from HIV-1 viremic patients. (A) Percentage of various TRAIL+ cell types in subgroups of patients infected with HIV-1. Healthy HIV-1–seronegative persons (n = 13) served as control group. Data are given as mean percentages of TRAIL+ cells minus isotype controls ± SEM. (B) Individual VLs as well as (C) counts of CD4+ T cells were correlated with the percentage of TRAIL-expressing pDCs. (D) Percentages of TRAIL-expressing pDCs were determined in 6 patients infected with HIV-1 before cART initiation and after 8 to 12 weeks, when the VL had fallen below the limit of quantification (< 50 RNA copies/mL plasma) in each case. (E) Isolated pDCs from HIV-negative donors were stimulated with (1) AT-2 HIV-1 plus an isotype control, (2) AT-2 HIV-1 plus a neutralizing anti–IFN-α antibody, and (3) matched microvesicles (MVs) plus isotype control for 12 hours and subsequently FACS stained for surface TRAIL expression. Data are given as mean percentages of TRAIL-positive pDCs minus isotype controls ± SEM of 2 independent experiments. (F) Representative histogram plots of indicated patient groups show the surface expression of TRAIL on freshly isolated pDCs compared with an isotype control (open lines). (G) TRAIL-expressing pDCs in different viral diseases: viremic patients infected with HIV-1 (n = 20), viremic patients infected with HCV (n = 10), patients infected with primary VZV (n = 4), and healthy controls (n = 13). Data are given as mean percentages of TRAIL-positive pDCs minus isotype controls ± SEM.

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