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. 2023 Aug 2;31(10):3067–3083. doi: 10.1016/j.ymthe.2023.07.024

Figure 5.

Figure 5

MSC treatment suppressed the activation of Th17 cells and secretion of TGF-β1

(A) Subclustering of lymphocytes from sham-, IRI-AKI-, and MSC-treated kidneys. (B) Relative contribution of each lymphocyte subtype in the sham-, IRI-AKI-, and MSC-treated groups. (C) The expression of the top 7 differentially expressed genes in each lymphocyte subtype. (D) Spearman’s correlation analysis showing the relationships between Th17 cell abundance and TEC subtype abundance. (E) Potential CD4 T cell differentiation routes revealed by trajectory analysis. (F) Heatmap showing the scaled expression of dynamic genes along the CD4 T cell trajectories. (G) Interaction analysis for immune cell subsets and TEC subsets showing significant receptor-ligand pairs. (H) The expression of ligand-receptor pairs genes in TCEs and immune cell subsets. (I) Representative immunofluorescence staining of the Th17 cell marker IL17A (red) in kidney sections from IRI-AKI (d 3)- and MSC-treated mice. (J) Flow cytometry plots showing the frequencies of CD45+CD3+CD8-IL17A+Th17 cells in IRI-3 d- and MSC-treated kidneys. (K) Levels of TGF-β1 in IRI-3 d- and MSC-treated kidneys, determined by ELISA. Data are expressed as mean ± SD (n = 3–6); Student’s t test was used for comparisons of two groups. ∗p < 0.05.