CD28 costimulation drives tumor-infiltrating T cell glycolysis to promote inflammation
CD28 costimulation drives tumor-infiltrating T cell glycolysis to promote inflammation
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DOI:
10.1172/jci.insight.138729
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发表时间:
2020-08-20
期刊:
影响因子:
8
通讯作者:
Rathmell, Jeffrey C.
中科院分区:
文献类型:
--
作者:
Beckermann, Kathryn E.;Hongo, Rachel;Rathmell, Jeffrey C.
Metabolic reprogramming dictates the fate and function of stimulated T cells, yet these pathways can be suppressed in T cells in tumor microenvironments. We previously showed that glycolytic and mitochondrial adaptations directly contribute to reducing the effector function of renal cell carcinoma (RCC) CD8(+) tumor-infiltrating lymphocytes (TILs). Here we define the role of these metabolic pathways in the activation and effector functions of CD8+ RCC TILs. CD28 costimulation plays a key role in augmenting T cell activation and metabolism, and is antagonized by the inhibitory and checkpoint immunotherapy receptors CTLA4 and PD-1. While RCC CD8(+) TILs were activated at a low level when stimulated through the T cell receptor alone, addition of CD28 costimulation greatly enhanced activation, function, and proliferation. CD28 costimulation reprogrammed RCC CD8(+) TIL metabolism with increased glycolysis and mitochondrial oxidative metabolism, possibly through upregulation of GLUT3. Mitochondria also fused to a greater degree, with higher membrane potential and overall mass. These phenotypes were dependent on glucose metabolism, as the glycolytic inhibitor 2-deoxyglucose both prevented changes to mitochondria and suppressed RCC CD8(+) TIL activation and function. These data show that CD28 costimulation can restore RCC CD8(+) TIL metabolism and function through rescue of T cell glycolysis that supports mitochondrial mass and activity.