Figure 7
Figure 7. Involvement of caspase-8 and caspase-9 in the CCL21-induced enhancement of AICD. Naive CD4+ T cells from BALB/c mice were stimulated with anti-CD3 and anti-CD28 mAbs for 4 days in the absence (−CCL21) or presence (+CCL21) of 100 ng/mL CCL21 in primary culture, and then restimulated with IL-2 alone or anti-CD3 mAb and IL-2 in secondary culture in the presence or absence of the pancaspase inhibitor (zVAD), caspse-8–specific inhibitor (IETD), or caspase-9–specific inhibitor (LEHD). Two days after, annexin V+PI− apoptotic cells were detected on flow cytometer. Caspase inhibitors were dissolved in DMSO and used at 100 μM. Where any inhibitors were not added, DMSO was used as a solvent control. Results are shown as mean ± SD of triplicate tests.

Involvement of caspase-8 and caspase-9 in the CCL21-induced enhancement of AICD. Naive CD4+ T cells from BALB/c mice were stimulated with anti-CD3 and anti-CD28 mAbs for 4 days in the absence (−CCL21) or presence (+CCL21) of 100 ng/mL CCL21 in primary culture, and then restimulated with IL-2 alone or anti-CD3 mAb and IL-2 in secondary culture in the presence or absence of the pancaspase inhibitor (zVAD), caspse-8–specific inhibitor (IETD), or caspase-9–specific inhibitor (LEHD). Two days after, annexin V+PI apoptotic cells were detected on flow cytometer. Caspase inhibitors were dissolved in DMSO and used at 100 μM. Where any inhibitors were not added, DMSO was used as a solvent control. Results are shown as mean ± SD of triplicate tests.

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