Skip to main content
. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Biochem Biophys Res Commun. 2020 Nov 13;534:773–779. doi: 10.1016/j.bbrc.2020.11.001

Figure 3. HDAC8 is upregulated in stimulated NK cells but not required for viability.

Figure 3.

(A) Transcriptional expression of HDACs during cytokine stimulation of primary human NK cells. RNA from freshly isolated human NK cells or NK cells stimulated with IL2, IL12, and IL18 for 24 hours were assessed by RT-qPCR. The data represents the average of 3 independent experiments with the error bars representing the standard deviation. *p<0.05. (B) Immunoblot of HDAC8 protein expression in primary NK and NK cell lines as indicated. (C) Viability of primary NK cells during HDAC8 inhibition. NK cells were treated with PCI-34051, vorinostat, or LBH-589 at the indicated concentration, followed by stimulation with IL2, IL12, and IL15. Viability was assessed by CTG at the times indicated and normalized to the vehicle (DMSO) control. Data represents the average of 3 independent experiments and error bars represent the standard deviation. (D) Viability of ex vivo expanded NK cells during HDAC8 inhibition. Lymphokine activated killer cells were expanded for 9 days, rested (100U/ml IL2) or subsequently reactivated (500U/ml IL2) overnight, followed by exposure to PCI-34051 at the indicated concentration. Viability was assessed as in panel C. Data represents the average of 2 independent experiments with the error bars representing the standard deviation.