期刊
CELL METABOLISM
卷 28, 期 3, 页码 504-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2018.06.002
关键词
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资金
- Deutscher Akademischer Austauschdienst (DAAD)
- Center for Infection Biology of the Hannover Biomedical Research School
- Ellen-Schmidt Program from the Medical School Hannover
- International Research Training Group 1273 from the Deutsche Forschungsgemeinschaft (DFG)
- DFG [LO1415 7-1]
- HiLF (MHH)
- DFG/ANR [SP615/12-1]
- CIHR [MOP-142259]
- FRQS
- Intramural Research Program of the NIH [HG200381-03]
- Braukmann-Wittenberg-Herz-Stiftung
- Deutsche Forschungsgemeinschaft
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [ZIAHG200381] Funding Source: NIH RePORTER
T cell subsets including effector (T-eff), regulatory (T-reg), and memory (T-mem) cells are characterized by distinct metabolic profiles that influence their differentiation and function. Previous research suggests that engagement of long-chain fatty acid oxidation (LC-FAO) supports Foxp3(+) T-reg cell and T-mem cell survival. However, evidence for this is mostly based on inhibition of Cpt1a, the rate-limiting enzyme for LC-FAO, with the drug etomoxir. Using genetic models to target Cpt1a specifically in T cells, we dissected the role of LC-FAO in primary, memory, and regulatory T cell responses. Here we show that the ACC2/Cpt1a axis is largely dispensable for T-eff, T-mem, or T-reg cell formation, and that the effects of etomoxir on T cell differentiation and function are independent of Cpt1a expression. Together our data argue that metabolic pathways other than LC-FAO fuel T-mem or T-reg differentiation and suggest alternative mechanisms for the effects of etomoxir that involve mitochondrial respiration.
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