Figure 3: Stimulation of CD40 induces activation of Akt. | Scientific Reports

Figure 3: Stimulation of CD40 induces activation of Akt.

From: Human IDO-competent, long-lived immunoregulatory dendritic cells induced by intracellular pathogen, and their fate in humanized mice

Figure 3

(A) MoDC and PDDC were suspended in 0.1% BSA in RPMI and then treated with anti-CD40 antibody. DCs were then treated with secondary antibody (sheep anti-mouse (Fab) 2 fragment antibody) for 15 min to induce clustering of CD40. The DCs were lysed and phosphorylated Akt1 was detected by using anti-Akt1 antibody. Well (1–3) loaded with DPG-PDDC ; well (4–5) loaded with MoDC. β-actin, loading control (n = 3) (B) model indicating a mechanism whereby the DPG-DC interaction may inhibit the apoptosis of DCs. Lower left panel, without DPG-DC interaction, transcription factor NF-kB, associated with its inhibitor IkB, and remains in the cytoplasm. On the contrary, pro-apoptotic factor FOXO1 from nucleus regulates the expression of pro-apoptotic family member Bim. Lower right panel, with DPG-DC interaction, CD40 located at the DPG-DC association induces activation of kinase Akt1. The activated Akt1 leads to, (1) phosphorylation by IkB, which is subsequently degraded, and allowing the translocation of NF-kB to the nucleus. NF-kB may control the transcription of pro-survival genes, and (2) phosphorylates FOXO1 in the nucleus and translocates it to cytoplasm which in turn inhibits the expression of Bim.

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