GSE169572
RNAseq data from WT and FOXO1-GFP null (KO) cytotoxic T lymphocytes (CTL) untreated or treated with PI3Kp110d inhibitor for 24hr
Phosphatidylinositol-3-kinase p110 delta (PI3Kp110d) is pivotal for CD8+ T cell immune responses. To inform how PI3Kp110d directs CD8+ T cell fate the current study focuses on PI3Kp110d controlled transcriptional programs and reveals how PI3Kp110d selectively induces and represses expression of key genes that create a cytotoxic T cell (CTL). The data identify differences in PI3Kp110d regulated transcriptional programs between naïve and effector cytotoxic T cells including differential control of cytolytic effector molecules, costimulatory receptors and the critical inhibitory receptors CTLA4 and SLAMF6. However, common to both naïve and effector cells is PI3Kp110d control of the production of chemokines and cytokines that orchestrate communication between the adaptive and innate immune system. The study provides a comprehensive resource for understanding how PI3Kp110d uses multiple processes  mediated by Protein Kinase B/AKT, FOXO1 dependent and independent mechanisms and mitogen-activated protein kinases (MAPK) to direct CD8+ T cell fate.  Overall design: mRNA profile of CTL from WT or FOXO1-GFP KO mice untreated or treated with PI3Kp110d inhibitor IC87114 for 24hr. 3 biological replicates for each condition.