期刊
NATURE IMMUNOLOGY
卷 14, 期 10, 页码 1064-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2687
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资金
- Swiss National Science Foundation [31003A_135677, 323630-128881, 323530-139181]
- Roche
- Swiss National Science Foundation (SNF) [323530-139181, 31003A_135677] Funding Source: Swiss National Science Foundation (SNF)
Antigen-experienced memory T cells acquire effector function with innate-like kinetics; however, the metabolic requirements of these cells are unknown. Here we show that rapid interferon-gamma (IFN-gamma) production of effector memory (EM) CD8(+) T cells, activated through stimulation mediated by the T cell antigen receptor (TCR) and the costimulatory receptor CD28 or through cognate interactions, was linked to increased glycolytic flux. EM CD8(+) T cells exhibited more glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity at early time points, before proliferation commenced, than did naive cells activated under similar conditions. CD28 signaling via the serine-threonine kinase Akt and the metabolic-checkpoint kinase mTORC2 was needed to sustain TCR-mediated immediate-early glycolysis. Unlike glycolysis in proliferating cells, immediate-early glycolysis in memory CD8(+) T cells was rapamycin insensitive. Thus, CD8(+) memory T cells have an Akt-dependent 'imprinted' glycolytic potential that is required for efficient immediate-early IFN-gamma recall responses.
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