Figure 5.
Figure 5. NFκB is involved in the antiapoptotic signaling induced from CCR7. (A) DCs were untreated (control) or pretreated with 20 mM n-acetyl-L-cysteine (NAC) or 20 μM SN50 for 60 minutes. Then, DCs were left unstimulated (–) or stimulated (+) with CCL19 or CCL21 for 6 hours. The percentage of annexin-positive/7-AAD–negative DCs was quantified. The data presented are representative of 2 independent experiments. (B) DCs untreated (control) or pretreated with LY294002 (100 μM) for 60 minutes were either left unstimulated (–) or stimulated (+) with CCL19 or CCL21 for an additional 30 minutes. (Top) DCs were taken to analyze by Western blotting the level of phosphorylated Akt1 (p-Akt) and subsequently, in the same blot, the levels of IκB. (Bottom) Blots were stripped and equal loading shown with an anti–β-actin antibody. A representative experiment out of 3 performed is shown.

NFκB is involved in the antiapoptotic signaling induced from CCR7. (A) DCs were untreated (control) or pretreated with 20 mM n-acetyl-L-cysteine (NAC) or 20 μM SN50 for 60 minutes. Then, DCs were left unstimulated (–) or stimulated (+) with CCL19 or CCL21 for 6 hours. The percentage of annexin-positive/7-AAD–negative DCs was quantified. The data presented are representative of 2 independent experiments. (B) DCs untreated (control) or pretreated with LY294002 (100 μM) for 60 minutes were either left unstimulated (–) or stimulated (+) with CCL19 or CCL21 for an additional 30 minutes. (Top) DCs were taken to analyze by Western blotting the level of phosphorylated Akt1 (p-Akt) and subsequently, in the same blot, the levels of IκB. (Bottom) Blots were stripped and equal loading shown with an anti–β-actin antibody. A representative experiment out of 3 performed is shown.

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