biostudies-literaturePatel CHNIAID NIH HHSHHS | NIH | National Institute of Biomedical Imaging and BioengineeringHHS | NIH | National Institute of Allergy and Infectious Diseases2287-2291https://www.ebi.ac.uk/biostudies/studies/S-EPMC10065985biostudies-literatureUnknown209(12)The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapamycin complex 2 signaling, represses memory CD8+ T cell differentiation. During acute infections, murine SGK1-deficient CD8+ T cells adopt an early memory precursor phenotype leading to more long-lived memory T cells. Thus, SGK1-deficient CD8+ T cells demonstrate an enhanced recall capacity in response to reinfection and can readily reject tumors. Mechanistically, activation of SGK1-deficient CD8+ T cells results in decreased Foxo1 phosphorylation and increased nuclear translocation of Foxo1 to promote early memory development. Overall, SGK1 might prove tJournal of immunology (Baltimore, Md. : 1950)Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1.PMC10065985P41EB028239R01AI07761R01 AI077610Wen JBlosser RLPatel CHSun IHTam AJPowell JDOh MHXu WSun IMHeikamp EBfalseCutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1.The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapamycin complex 2 signaling, represses memory CD8+ T cell differentiation. During acute infections, murine SGK1-deficient CD8+ T cells adopt an early memory precursor phenotype leading to more long-lived memory T cells. Thus, SGK1-deficient CD8+ T cells demonstrate an enhanced recall capacity in response to reinfection and can readily reject tumors. Mechanistically, activation of SGK1-deficient CD8+ T cells results in decreased Foxo1 phosphorylation and increased nuclear translocation of Foxo1 to promote early memory development. Overall, SGK1 might prove t2022-01-01T00:00:00Z2022 Dec2025-04-04T11:20:56.657Z2025-04-04T11:20:56.657ZS-EPMC100659853646984410.4049/jimmunol.2100669