Metabolic control of regulatory T cell (Treg) survival and function by Lkb1

Significance Regulatory T cells (Tregs) play a critical role in maintaining immune tolerance to self-antigens and in suppressing excessive immune responses that may cause collateral damage to the host. Unlike other CD4 + T cells, Tregs have a distinct, yet-to-be-established metabolic machinery to produce energy for survival and function. Here we show that the metabolic sensor LKB1 is critical for the survival and function of Tregs through regulation of their cellular metabolism. Interestingly, AMP-activated protein kinase, the best-studied downstream kinase of LKB1, is largely dispensable for LKB1 function in Tregs; the MAP/microtubule affinity-regulating kinases and salt-inducible kinases may mediate its functions. We highlight LKB1 as metabolic regulator that links cellular metabolism to immune cell functions.