Figure 5.
Figure 5. CpG-A and IL-15 in combination induce maximal activation of patients' NK cells. (A) PBMCs from SS patients (n = 11, ▪) and healthy volunteers (n = 7, ▦) were stimulated with CpG-A, control CpG ODN, IL-15 (1 ng/mL), or the combination of CpG-A and IL-15 as described in Figure 2. Cells were then harvested, stained with appropriate antibodies, and analyzed for the expression of CD69 on CD56 NK cells. Data represent means (± SD) of tested individuals and are presented as a percentage of CD56 NK cells expressing CD69. *P < .05 compared with IL-15 or CpG-A. (B) PBMCs from low to medium tumor burden patients (n = 5, left panel) and high tumor burden patients (n = 4, right panel) were stimulated with CpG-A, control CpG ODN, IL-15, or the combination of CpG-A and IL-15 as described in Figure 2, followed by a 4 hours' Cr51 release assay using K562 cells as targets. Data represent means (± SD) of tested individuals and are presented as a percentage of specific lysis.

CpG-A and IL-15 in combination induce maximal activation of patients' NK cells. (A) PBMCs from SS patients (n = 11, ▪) and healthy volunteers (n = 7, ▦) were stimulated with CpG-A, control CpG ODN, IL-15 (1 ng/mL), or the combination of CpG-A and IL-15 as described in Figure 2. Cells were then harvested, stained with appropriate antibodies, and analyzed for the expression of CD69 on CD56 NK cells. Data represent means (± SD) of tested individuals and are presented as a percentage of CD56 NK cells expressing CD69. *P < .05 compared with IL-15 or CpG-A. (B) PBMCs from low to medium tumor burden patients (n = 5, left panel) and high tumor burden patients (n = 4, right panel) were stimulated with CpG-A, control CpG ODN, IL-15, or the combination of CpG-A and IL-15 as described in Figure 2, followed by a 4 hours' Cr51 release assay using K562 cells as targets. Data represent means (± SD) of tested individuals and are presented as a percentage of specific lysis.

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