Fig. 3.
Escape from apoptosis of TNF-+ T cells is associated with cosynthesis of IL-2.
Following 16 hours of PMA+PHA+ionomycin stimulation, dual intracellular staining of PBMCs was performed with anti–IL-2-PE and anti–TNF-α-FITC mAbs. (A) Dot-plots, gated on CD3+ T cells, from a representative HIV− control, an HIV+ PI− patient (M0), and an HIV+ PI+ patient treated for 12 months (M12). (B) Differential susceptibility to activation-induced apoptosis of IL-2+TNF-α−, IL-2+TNF-α+, and IL-2−TNF-α+ lymphocytes. (C) Relative contribution of IL-2+TNF-α+ and IL-2−TNF-α+ cells to the expansion of total TNF-α+ T cells following HAART. The letter C indicates healthy subjects (n = 7); PI−, HIV+ PI− patients naı̈ve of PI therapy (n = 12); and PI+, HIV+ PI+patients with at least 9 months of PI therapy (n = 13). Paragraph symbol indicates P < .05 vs HIV− controls; asterisk, P < .05 vs HIV+ PI− patients (Mann-Whitney U test).