Nutrient inputs and social metabolic control of T cell fate

被引:6
作者
Bacigalupa, Zachary A. [1 ,2 ]
Landis, Madelyn D. [1 ]
Rathmell, Jeffrey C. [2 ,3 ]
机构
[1] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Immunobiol, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Dept Pathol Microbiol & Immunol, Nashville, TN 37232 USA
关键词
ACETYL-COA SYNTHETASE; HISTONE ACETYLATION; O-GLCNAC; GLUTAMINE UPTAKE; METHYLENETETRAHYDROFOLATE REDUCTASE; POSTTRANSLATIONAL MODIFICATIONS; SIGNALING PATHWAY; GENE-EXPRESSION; INSULIN; COMPLEX;
D O I
10.1016/j.cmet.2023.12.009
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cells in multicellular organisms experience diverse neighbors, signals, and evolving physical environments that drive functional and metabolic demands. To maintain proper development and homeostasis while avoiding inappropriate cell proliferation or death, individual cells interact with their neighbors via "social"cues to share and partition available nutrients. Metabolic signals also contribute to cell fate by providing biochemical links between cell-extrinsic signals and available resources. In addition to metabolic checkpoints that sense nutrients and directly supply molecular intermediates for biosynthetic pathways, many metabolites directly signal or provide the basis for post-translational modifications of target proteins and chromatin. In this review, we survey the landscape of T cell nutrient sensing and metabolic signaling that supports proper immunity while avoiding immunodeficiency or autoimmunity. The integration of cell-extrinsic microenvironmental cues with cell-intrinsic metabolic signaling provides a social metabolic control model to integrate cell signaling, metabolism, and fate.
引用
收藏
页码:10 / 20
页数:11
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