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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: The activation of PPARγ enhances Treg responses through up-regulating CD36/CPT1-mediated fatty acid oxidation and subsequent N-glycan branching of TβRII/IL-2Rα

Fig. 3

The Treg-promoting effect of PPARγ agonists is dampened by knocking down CD36/CPT1. a, b The naïve CD4+ T cells were transfected with siCD36 or siCPT1, and the protein levels of CD36 (a) and CPT1 (b) were detected by western blotting. c, d 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 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 < 0.05, &&P < 0.01 versus 15d-PGJ2 group; P < 0.05 versus morin group

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