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

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

Background: Peroxisome proliferator-activated receptor gamma (PPARγ) is an enhancer of Treg responses, but the mechanisms remain elusive. This study aimed to solve this problem in view of cellular metabolism. Methods: Three recognized PPARγ agonists (synthetic agonist: rosiglitazone; endogenous liga...

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Bibliographic Details
Main Authors: Dai, Y. (Author), Hu, Y. (Author), Miao, Y. (Author), Wei, Z. (Author), Xue, X. (Author), Yang, L. (Author), Zeng, X. (Author), Zhang, C. (Author)
Format: Article
Language:English
Published: BioMed Central Ltd 2022
Subjects:
CD36/CPT1
Fatty acid oxidation
PPARγ
Treg responses
UDP-GlcNAc/glycosylation
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