Fig. 7

Surface retention of TβRII/IL-2Rα resulting from glycosylation links PPARγ agonists-boosted FAO and Treg responses. a The naïve CD4⁺ T cells were transfected with siCD36 or siCPT1, 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) for 48 h. The cell surface levels of TβRII and IL-2Rα (CD25) were analyzed by flow cytometry. b–d The naïve CD4⁺ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of TGF-β (5 ng/mL), tunicamycin (1 μM), rosiglitazone (30 μM), 15d-PGJ2 (10 μM) as well as morin (30 μM). After 48 h, the cell surface levels of TβRII and IL-2Rα (CD25) (b) were analyzed by flow cytometry. After 72 h, the frequency of CD4⁺Foxp3⁺ T cells was examined by flow cytometry (c) and the mRNA expression level of Foxp3 was measured by Q-PCR (d). 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 < 0.01 versus TGF-β group (model group); ^$P < 0.05, ^$$P < 0.01 versus rosiglitazone group; ^&&P < 0.01 versus 15d-PGJ2 group; ^††P < 0.01 versus morin group