<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE287nnn/GSE287743/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Mus musculus</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE287743</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>In vitro PI3Kδ inhibition skews CD8 T cell differentiation towards progenitor exhaustion in vivo and reprograms tumor microenvironment metabolism, immune composition, and inflammation [Spatial Transcriptomics]</name><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.</description><dates><publication>2026/06/03</publication></dates><accession>GSE287743</accession><cross_references><GSM>GSM8750729</GSM><GSM>GSM8750728</GSM><GSM>GSM8750730</GSM><GSM>GSM8750732</GSM><GSM>GSM8750731</GSM><GSM>GSM8750733</GSM><GPL>30172</GPL><GSE>287743</GSE><taxon>Mus musculus</taxon><PMID>[42215073]</PMID></cross_references></HashMap>