Fig. 9

The regulation of PPARγ agonists on CD36/CPT1-mediated FAO and Treg responses exerts a PPARγ-dependent feature. a The naïve CD4⁺ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of TGF-β (5 ng/mL), rosiglitazone (10, 30 μM), 15d-PGJ2 (3, 10 μM) as well as morin (10, 30 μM) for 48 h. The binding of PPARγ to the promoter of CD36/CPT1 was detected by ChIP assay. b, c The naïve CD4⁺ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of TGF-β (5 ng/mL), actinomycin D (Act-D; 1 μM), rosiglitazone (30 μM), 15d-PGJ2 (10 μM) as well as morin (30 μM) for 48 h. The mRNA expression levels of CD36 and CPT1 were measured by Q-PCR (b), and the protein levels of CD36 and CPT1 were detected by western blotting (c). d–j The naïve CD4⁺ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of TGF-β (5 ng/mL), GW9662 (1 μM), rosiglitazone (30 μM), 15d-PGJ2 (10 μM) as well as morin (30 μM). After 48 h, the mRNA expression levels of CD36 (d) and CPT1 (e) were measured by Q-PCR. After 72 h, the frequency of CD4⁺Foxp3⁺ T cells was examined by flow cytometry (f), and the mRNA expression levels of Foxp3 (g), IL-10 (h), CTLA4 (i) and TIGIT (j) were measured by Q-PCR. k–n The naïve CD4⁺ T cells were transfected with PPARγ KO plasmid and treated with anti-CD3/CD28 in the presence or absence of TGF-β (5 ng/mL), rosiglitazone (30 μM), 15d-PGJ2 (10 μM) as well as morin (30 μM). After 48 h, the mRNA expression levels of CD36 (k) and CPT1 (l) were measured by Q-PCR. After 72 h, the frequency of CD4⁺Foxp3⁺ T cells was examined by flow cytometry (m), and the mRNA expression level of Foxp3 (n) was measured by Q-PCR. Data were presented as the means ± S.E.M. of three independent experiments (n = 3). ^#P < 0.05, ^##P < 0.01 versus control group; *P < 0.05, **P < 0.01 versus TGF-β group (model group); ^$P < 0.05, ^$$P < 0.01 versus rosiglitazone group; ^&P < 0.05, ^&&P < 0.01 versus 15d-PGJ2 group; ^†P < 0.05, ^††P < 0.01 versus morin group