{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE333nnn/GSE333230/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Genome binding/occupancy profiling by high throughput sequencing","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333230"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"The Transcription Factor IRF8 drives tumor-specific exhaustion in CD8 T cells","description":"T-cell exhaustion is a hallmark of chronic infection and cancer and constitutes a major barrier for successful immunotherapies. In this study, we establish the central role of IRF8 as a transcription factor regulating tumor-induced T cell exhaustion. IRF8 is highly expressed in CD8 T cells in tumors but not during chronic infection, where the Irf8 locus is less accessible. Its expression depends on TCR stimulation but is altered in the presence of type I IFN. Overexpression of IRF8 strongly enforced T cell dysfunction while IRF8 knock-out in tumor specific CD8 T cells reduced TOX expression and ameliorated effector function by increasing IFNγ, GrzB and TNF production, resulting in a better tumor control. By comparing IRF8 to IRF2 and IRF4, we showed that the IRF family display some redundancy in the regulation of T cell exhaustion converging on TOX-dependent programs. Altogether, we established a new role for IRF8 as a tumor specific regulator of T cell function.","dates":{"publication":"2026/06/05"},"accession":"GSE333230","cross_references":{"GSM":["GSM9759609","GSM9759605","GSM9759606","GSM9759607","GSM9759608","GSM9759601","GSM9759602","GSM9759603","GSM9759604","GSM9759610","GSM9759599","GSM9759600"],"GPL":["34475"],"GSE":["333230"],"taxon":["Mus musculus"]}}