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Rapamycin Modulate Treg/Th17 Balance via Regulating Metabolic Pathways: A Study in Mice
Jiabi Zhang1, Hong Jin2, Yan Xu2
1Chengdu Medical College, Chengdu, Sichuan Province, PR China; Department of Laboratory Medicine, West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, PR China; Key Laboratory of Obstetric & Gynecologic and Pediatric Disease and Birth Defects of Ministry of Education, Chengdu, Sichuan Province, PR China.
Transplantation Proceedings
|August 11, 2019
Summary
Rapamycin (Rapa) rebalances regulatory T (Treg) and T helper 17 (Th17) cells by blocking glycolysis in Th17 cells and promoting fatty acid oxidation in Treg cells, offering insights into autoimmune disease treatment.
Area of Science:
- Immunology
- Cell Biology
- Metabolic Pathways
Background:
- Treg/Th17 cell imbalance is implicated in autoimmune diseases.
- Rapamycin (Rapa) influences Treg and Th17 cell differentiation.
Purpose of the Study:
- To elucidate the mechanism by which Rapamycin (Rapa) modulates Treg and Th17 cell differentiation.
- To investigate the metabolic reprogramming induced by Rapa in these T cell subsets.
Main Methods:
- Purified mouse CD4+CD25- T cells were polarized in vitro into Th17 or Treg cells with or without Rapa.
- Metabolic pathways, including glycolysis and fatty acid oxidation (FAO), were analyzed in Rapa-treated cells.
Main Results:
- Rapa inhibited Th17 cell differentiation and promoted Treg cell generation.
- Rapa blocked glycolysis in Th17 cells by reducing glucose uptake and inhibiting key glycolytic enzymes and transcription factors (c-Myc, HIF-1α).
- Rapa promoted fatty acid oxidation (FAO) in Treg cells, increasing FAO products and key enzymes (ATGL, CPT1A), and activating phospho-AMPKα.
Conclusions:
- Rapamycin differentially regulates T cell metabolism, inhibiting glycolysis in Th17 cells and enhancing FAO in Treg cells.
- These metabolic shifts likely underlie Rapa's ability to restore Treg/Th17 balance, offering potential therapeutic strategies for autoimmune diseases.
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