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. Author manuscript; available in PMC: 2019 May 28.

Published in final edited form as: Leukemia. 2018 Feb 22;32(9):1932–1947. doi: 10.1038/s41375-018-0062-8

Fig. 7 — Increased AKT/mTOR/NF-κB p65 activation and Bcl-6, HIF1, Eomes and T-bet expression in memory CD8⁺ T cells of XBP1 antigen-specific CTL triggered by ACY241 treatment. XBP1-CTL were evaluated for the effects of ACY241 treatment on the AKT (pS473)/mTOR (pS2448)/NF-κB p65 pathways and the Bcl-6, HIF1, Eomes and T-bet expression. ACY241 treatment enhanced the activation levels of AKT, mTOR and p65, mainly within the memory cell subsets in the XBP1-CTL (Fig. 7a). In addition, ACY241 treatment enhanced the expression of key transcriptional regulators Bcl-6, HIF1, Eomes and T-bet in XBP1-CTL (Fig. 7b), which was detected mainly within memory T cell subset (p <0.05) (Fig. 7c)

Fig. 7 — Increased AKT/mTOR/NF-κB p65 activation and Bcl-6, HIF1, Eomes and T-bet expression in memory CD8⁺ T cells of XBP1 antigen-specific CTL triggered by ACY241 treatment. XBP1-CTL were evaluated for the effects of ACY241 treatment on the AKT (pS473)/mTOR (pS2448)/NF-κB p65 pathways and the Bcl-6, HIF1, Eomes and T-bet expression. ACY241 treatment enhanced the activation levels of AKT, mTOR and p65, mainly within the memory cell subsets in the XBP1-CTL (Fig. 7a). In addition, ACY241 treatment enhanced the expression of key transcriptional regulators Bcl-6, HIF1, Eomes and T-bet in XBP1-CTL (Fig. 7b), which was detected mainly within memory T cell subset (p <0.05) (Fig. 7c)