Figure 2. A metabolically distinct subset of T cells with low VDAC1 and low p-S6 expression increases in kidneys following ischemic AKI.

(A) Schematic of the experimental design. (B) Concatenated flow cytometry data depicted as UMAP of T cells in control kidneys, ischemic kidneys, and post-IRI kidneys. Post-IRI kidneys showed distinct segregated populations having low VDAC1 and p-S6 expressions compared with the control kidneys and ischemic kidneys. (C) Representative flow plots showing VDAC1^lop-S6^lo T cells. Frequencies of VDAC1^lop-S6^lo subsets among CD4⁺, CD8⁺, and DN T cells in mouse kidneys. They were significantly increased following reperfusion. Statistical analyses were performed using 1-way ANOVA followed by Tukey’s post hoc analysis (n = 10 mice in each group). Data are from 2 independent experiments. (D) Histograms comparing VDAC1^lop-S6^lo T cells (blue) and remaining T cells (brown) from concatenated post-IRI 48 hours data. (E) Changes in glycolysis enzymes on VDAC1^lop-S6^lo T cells according to different time points. GLUT1 and HKII on those cells were increased significantly following IRI. Statistical analyses were performed using 2-way ANOVA followed by Tukey’s post hoc analysis (n = 10 mice in each group). Data are from 2 independent experiments. *P < 0.05, compared with the control group; †P < 0.05, compared with the ischemia group; ^¶P < 0.05, compared with the post-IRI 4 hours group. CPT1a, carnitine palmitoyltransferase 1a; DN, double-negative; IRI, ischemia/reperfusion injury; MFI, mean fluorescence intensity; pS6, phosphorylated ribosomal protein S6; UMAP, uniform manifold approximation and projection; VDAC1, voltage-dependent anion channel 1.