responses, while SREBP1 was shown to mediate changes in the activity of the pentose

phosphate pathway and lipid biosynthesis in mouse embryonic fibroblasts [31]. Using a

variety of mTORC1- and mTORC2-deficient T cell systems, several groups have previously shown that mTOR regulates Th1, Th2, Th17, and Treg differentiation [40–44]. Furthermore, mTOR also has been shown to regulate CD8+ memory formation [45].AMPK is another regulator of T cell metabolism and function that also has well-defined

mammalian Target of Rapamycin (mTOR), modulate nutrient uptake as well as expression and activity of metabolic enzymes [8, 31–36]. Notably, these regulators have dual roles in the regulation of both T cell metabolism and function [8]. Moreover, some of them, such as mTOR and APMK, have well-defined roles in the regulation of macroautophagy [33, 37– 39], which supports a common link among the regulation of T cell function, metabolism, and macroautophagy.