Fig. 4

DCA increases the generation of endogenous RORγt agonists. a Schematic view of cholesterol synthetic pathways. Inhibitors used in b was shown in red. b CD4⁺ T cells were differentiated under Th0 or Th17-polarizing conditions in the absence or presence of DCA (100 µM). CYP51 inhibitor ketoconazole (1 µM) or cholesterol biosynthesis inhibitor lovastatin (10 µM) was added 30 min ahead of DCA treatment. The percentages of IL-17-producing CD4⁺ T cells were analyzed by flow cytometry. c Relative levels of cholesterol biosynthesis precursors in untreated and DCA-treated EL4 cells measured by LC–MS (n = 3). d Comparison of zymosterol, desosterol and lanosterol concentrations in untreated and DCA-treated EL4 cells (n = 3). Two-tailed Student’s t-tests were used. Data are expressed as mean ± SEM from at least three independent experiments or representative data (b)