GSE169436
RNAseq data for ex vivo Naïve CD8+ T cells and TCR activated 24hr in the presence or absence of PI3Kp110d inhibitor
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 ex vivo CD8+ T cells, 24hr activated in the presence or absence of PI3Kp110d inhibitor IC87114. 3 biological replicates for each condition.The dataset includes also a group of 6 samples (number 10 to 15) which were run on the same RNAseq lane but are not part of the manuscript.