{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308060/"]},"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=GSE308060"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Epigenetic control of CD8+ T cell tissue resident memory precursors differentiation by the histone methyltransferase SUV39H1","description":"The molecular mechanisms of fate choices between circulatory and tissue-resident memory (TRM) cells upon CD8+ T cell activation, are still largely unknown. We show here that deletion of the histone methyltransferase SUV39H1 in CD8+ T cells, enhances homing to non-lymphoid tissues. At steady state, after space-induced proliferation or flu infection, SUV39H1-defective cells in tissues express CD49d and differentiate predominantly into CD69+/CD103- TRM. Persisting SUV39H1-defective T cells in lungs are protective in flu re-infection and lung tumor models. Accumulation of SUV39H1-deficient TRM cells is due to increased proportions of TRM precursors with high stemness and TRM precursor potential. We conclude that SUV39H1 restrains CD69+ CD103- TRM commitment by inhibiting memory and stemness programs during CD8+ T cells effector differentiation. These results encourage the use of SUV39H1 depletion in the context of adoptive T cell therapies to optimize both the efficiency of target cell eradication and the long-term persistence of memory cells.","dates":{"publication":"2026/09/14"},"accession":"GSE308060","cross_references":{"GSM":["GSM9237323","GSM9237324","GSM9237325"],"GPL":["24247"],"GSE":["308060"],"taxon":["Mus musculus"]}}