Fig. 8From: The activation of PPARγ enhances Treg responses through up-regulating CD36/CPT1-mediated fatty acid oxidation and subsequent N-glycan branching of TβRII/IL-2RαThe increased cell surface level of CD36 is mainly attributed to the regulation of its overall expression by PPARγ agonists. a, b The naïve CD4+ T cells were prepared and treated with anti-CD3/CD28 in the presence or absence of GlcNAc (10, 20, 40, 80 mM) for 48 h. The cell surface level of CD36 were analyzed by flow cytometry (a), and the mRNA expression level of CD36 was measured by Q-PCR (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), rosiglitazone (10, 30 μM), 15d-PGJ2 (3, 10 μM) as well as morin (10, 30 μM) for 48 h. The cell surface level of CD36 was analyzed by flow cytometry. d, e 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) for 48 h. The cell surface level of CD36 was analyzed by flow cytometry (d), and the mRNA expression level of CD36 was measured by Q-PCR (e). f The naïve CD4+ T cells were transfected with siCD36, 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 level of CD36 was analyzed by flow cytometry. 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 groupBack to article page