Fig. 7

Fluvoxamine represses Th1 and Th17 differentiation and glycolysis by regulating the PI3K/AKT axis. A Genes downregulated in fluvoxamine-treated CD4⁺ T were subjected to KEGG pathway enrichment analysis. B Results for Gene Set Enrichment Analysis (GSEA) of PI3K-AKT signaling pathways. C, D The purified CD4⁺ T cells were cultured with fluvoxamine (0 μM, 5 μM, 10 μM) for 24 h. The protein expression of p-PI3K, p-AKT, PI3K and AKT was assessed. CD4⁺ T cells were cultured with fluvoxamine, vehicle or PI3K activator 740 Y-P for 24 h and E ECAR was analyzed by an extracellular flux analyzer. F Results for glycolysis and glycolytic capacity in CD4⁺ T cells with different treatment. G and H Naïve CD4⁺ T cells isolated from spleen were exposed to Th1-or Th17- inducing conditions under indicated culture conditions. G Th1 and H Th17 polarization efficiency were analyzed by flow cytometry. Each dot represents the mean of three biological replicates. Data are expressed as mean ± SEM. Significance was determined by one-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, and ns, not significant