{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE324nnn/GSE324468/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Mus musculus"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE324468"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Targeting E-Proteins Licenses cDC1 Immunogenicity for Potent Anti-Tumor Vaccination [ChIP-seq]","description":"Type 1 conventional dendritic cells (cDC1s) are essential for priming anti-tumor CD8⁺ T cells, yet the intrinsic pathways limiting their function remain unclear. Here we identify E-proteins (E2A/HEB) as a master checkpoint that actively suppresses cDC1 immunogenicity by directly transactivating PTEN, thereby restraining PI3K-AKT-mTOR signaling, FLT3L-driven proliferation, and NF-κB-mediated IL-12 production. Genetic ablation of E-proteins in DCs unleashes a hyperfunctional program—expanded cDC1 populations, enhanced antigen presentation, and superior CD8⁺ T cell priming—while deletion of the E-protein antagonist Id2 impairs cDC1 function, establishing a bidirectional rheostat. This axis is clinically relevant, as dynamic E-protein activity in human tumor DCs correlates with patient survival and response to immune checkpoint blockade. Finally, vaccination with E-protein-deficient DCs elicits potent antigen-specific T cell expansion and achieves robust therapeutic efficacy across multiple preclinical tumor models, defining a targetable checkpoint and establishing E-protein inactivation as a platform for next-generation cancer immunotherapies.","dates":{"publication":"2026/03/15"},"accession":"GSE324468","cross_references":{"GSM":["GSM9577984","GSM9577983"],"GPL":["24247"],"GSE":["324468"],"taxon":["Mus musculus"]}}