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. 2022 Mar 2;13(6):1805–1827. doi: 10.1016/j.jcmgh.2022.02.019

Figure 9.

Figure 9

AA regulatesTCRγδ+DNT cells function via NF-κB signaling pathway. (A) Distributions of differential genes with up-regulated (907) and down-regulated (438) expression in AA-treated TCRγδ+ DNT cells and control; fold change ≤ 0.5 or fold change ≥ 1.5; P < .05. n = 3/group. (B) Biological Process analysis was performed on basis of differential genes with significantly up-regulated and down-regulated expression in AA-treated TCRγδ+ DNT cells and control. (C and D) Heatmap showing the genes related to apoptotic process and inflammatory response in AA-treated TCRγδ+ DNT cells and control. (E) Heatmap showing expression of NF-κB signaling pathway in AA-treated TCRγδ+ DNT cells and control. (F) P-AKT, P50, and P-IKBα expression in TCRγδ+ DNT cells after AA stimulation. n = 6 biologically independent samples per group. (G) Apoptosis, Bodipy, P-IKBα, and IL17A expression in TCRγδ+ DNT cells after treating with AA and NF-κB inhibitor BAY 11-7082. n = 6 biologically independent samples per group. (H) The TFBSs in the upstream region (2k base pairs upstream from the transcription starting site) and downstream region (100 base pairs downstream from the transcription starting site) of Il17a were predicted. (I) Real-time PCR verified the expression of Nfkb2 in AA-treated TCRγδ+ DNT cells and control. n = 6 biologically independent samples per group. (J) Real-time PCR verified the expression of Nfkb2 in TCRγδ+ DNT cells in NAFLD and normal mice livers. n = 5 biologically independent samples per group. Two-sided P values <.05 were considered significant. ∗∗P < .01; ∗P < .05.