Linking Innate and Adaptive Immunity: Human V9V2 T Cells Enhance CD40 Expression and HMGB-1 Secretion
Figure 2
Modulation of CD40, CD86, HLA-DR and CD80 on APCs by IPP-activated γ δ T cells. PBMC were cultured overnight in the presence of IPP or absence of IPP before stimulation with 1 nM of TSST-1 (a). Data (mean SEM) for expression of CD40, CD86, HLA-DR and CD80 were shown after various time intervals following TSST-1 stimulation, and the numbers of healthy donors studied for each co-receptor are as indicated. Baseline values were obtained from PBMC treated with RPMI growth medium alone. To determine the influence of IPP-activated γ δ T cells on receptor expression following TSST-1 stimulation, comparisons were made between IPP + TSST-1 (dashed red lines) versus TSST-1 alone (solid black line), and significant differences were denoted by (). To confirm that any observed difference in receptor expression was due to the presence of activated γ δ T cells, a cognate group of PBMC were depleted of γ δ T cells () and studied in parallel experiments (b). To determine the influence of TSST-1 on IPP-activated γ δ T cells, comparisons were made between IPP + TSST-1 versus IPP alone. Overnight IPP treatment significantly up-regulated CD40 expression at 3hours and 6hours after TSST-1 stimulation (, student’s test), and down-regulated CD86 expression at 3h after TSST-1 stimulation (). No other significant differences in receptor expression were observed for the other co-stimulatory molecules.
