Metabolism, migration and memory in cytotoxic T cells

被引:190
作者
Finlay, David [1 ]
Cantrell, Doreen A. [1 ]
机构
[1] Univ Dundee, Div Cell Biol & Immunol, Dundee, Scotland
基金
英国惠康基金;
关键词
ACTIVATED PROTEIN-KINASE; FORKHEAD TRANSCRIPTION FACTOR; PHOSPHATIDYLINOSITOL; 3-KINASE; PHOSPHOINOSITIDE; IMMUNOLOGICAL SYNAPSE; GLUCOSE DEPRIVATION; MEDIATED CYTOLYSIS; SIGNALING PATHWAYS; EFFECTOR FUNCTIONS; ENERGY-METABOLISM;
D O I
10.1038/nri2888
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The transcriptional and metabolic programmes that control CD8(+) T cells are regulated by a diverse network of serine/threonine kinases. The view has been that the kinases AKT and mammalian target of rapamycin (mTOR) control T cell metabolism. Here, we challenge this paradigm and discuss an alternative role for these kinases in CD8(+) T cells, namely to control cell migration. Another emerging concept is that AMP-activated protein kinase (AMPK) family members control T cell metabolism and determine the effector versus memory fate of CD8(+) T cells. We speculate that one link between metabolism and immunological memory is provided by kinases that originally evolved to control T cell metabolism and have subsequently acquired the ability to control the expression of key transcription factors that regulate CD8(+) T cell effector function and migratory capacity.
引用
收藏
页码:109 / 117
页数:9
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