{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE286nnn/GSE286925/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Other","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE286925"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"In vitro PI3Kδ inhibition skews CD8 T cell differentiation towards progenitor exhaustion in vivo and reprograms tumor microenvironment metabolism, immune composition, and inflammation [scRNA-seq]","description":"In vitro PI3Kδ inhibition using Idelalisib (CAL-101) drives CD8 T cells toward a progenitor exhausted (Tpex) phenotype while resisting terminal exhaustion in vitro. We performed single-cell RNA sequencing and spatial transcriptomics on B16-melanoma tumors and show that CAL-101-treated T cells enhance oxidative phosphorylation, proliferation, and Ifnγ responsiveness. The CAL-101 treated cells deeply infiltrate tumors and upregulate the CXCR3-CXCL10 axis, coinciding with reduced tumor-associated macrophage signatures and increased pro-inflammatory signaling in the tumor microenvironment. CAL-101 reprograms T cell fate and remodels the TME, offering insight into how to improve immunotherapeutic efficacy for solid tumors.","dates":{"publication":"2026/06/03"},"accession":"GSE286925","cross_references":{"GSM":["GSM8734426","GSM8734425","GSM8734424","GSM8734423","GSM8734422","GSM8734432","GSM8734421","GSM8734431","GSM8734430","GSM8734429","GSM8734428","GSM8734427"],"GPL":["30172"],"GSE":["286925"],"taxon":["Mus musculus"],"PMID":["[42215073]"]}}