Fig. 5 | Scientific Reports

Fig. 5

From: CD38 modulates cytokine secretion by NK cells through the Sirt1/NF-κB pathway, suppressing immune surveillance in colorectal cancer

Fig. 5

The effect of CD38-mediated Sirt1/NF-κB signaling on cytokine secretion and the resultant modulation of CD4 + T-cell differentiation. Expression levels of NF-κB and acetyl-NF-κB proteins in CD38 + NK cells treated with RSV (Sirt1 activator) or DMSO (A) and quantitation for NF-κB (B) and acetyl-NF-κB (C). Expression levels of NF-κB and acetyl-NF-κB proteins in CD38 + NK cells treated with NAM (Sirt1 inhibitor) or DMSO (D) and quantitation for NF-κB (E) and acetyl-NF-κB (F). (G) Acetyl-NF-κB expression was compared with NF-κB expression. (H) Cytokine levels in the culture supernatant of CD38 + NK cells treated with PDTC (NF-κB inhibitor) or PBS. (I). CD4 + T cells were cocultured with CD38 + NK cells pretreated with PDTC or PBS. (J). Proportions of Tregs, Th1, Th2, and Th17 cells and the ratios of Th17/Treg and Th1/Th2 cells among CD4 + T cells cocultured with CD38 + NK cells that were pretreated with PDTC or PBS. CD38 + NK (HC): CD38 + NK cells isolated from the blood of healthy controls; CD38 + NK (CRC): CD38 + NK cells isolated from the blood of CRC patients; CRC cells: colorectal cancer; RSV: resveratrol; NAM: nicotinamide; DMSO: dimethyl sulfoxide. ns: not statistically significant; *: P < 0.05, **: P < 0.01 and ***: P < 0.001.

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