Fig. 2: PPARγ and lipid synthesis promote activation and IFN-γ production of iNKT cells.

a, b Surface CD69 (a), CD25 (b) on iNKT cells after activating by plate-coated anti-CD3 and anti-CD28 in the absence or presence of T007, Tofa. Unstimulated iNKT cells were used as negative controls. c Frequencies of Ki67⁺ iNKT cells after activating with plate-coated anti-CD3 and anti-CD28 for 2 days with or without T007, Tofa. d IFN-γ and IL-4 production in iNKT cells activated by plate-coated mCD1d-PBS57 tetramer in the absence or presence of T007. e IFN-γ and IL-4 production in iNKT cells in the absence or presence of Tofa as described in d. f, g mRNA of Ifng and Il4 in iNKT cells activated by anti-CD3 plus anti-CD28 for 24 h with or without antagonists of PPARγ (f) or fatty acid synthesis inhibitors (g). h, i Knockdown efficiency of Pparg shRNA (h) and its effect on percentages of IFN-γ⁺ iNKT cells, after activating with plate-coated anti-CD3 and anti-CD28 (i). j PPARγ expression in iNKT cells or T cells from PLZF-cre Pparg^fl/fl mice or Pparg^fl/fl mice. k Percentages of IFN-γ⁺ iNKT cells from PLZF-cre Pparg^fl/fl mice or Pparg^fl/fl mice, after activating with plate-coated anti-CD3 and anti-CD28 with or without T007, or PIO. Data are representative of six mice (j), or are means ± SEM of three independent experiments (h, i), nine biological replicates (a–e), four independent experiments (f, g), or six mice (k), pooled from three to four independent experiments. Data were analyzed by unpaired Student’s t-test (a–e) or Mann-Whitney test (f–i, k). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Source data are provided as a Source Data file.