{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE284nnn/GSE284445/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE284445"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Cytotoxic Tissue-Resident NK Cells Infiltrate and Control Solid Epithelial Tumor Growth [ATAC-Seq]","description":"Human tissue-resident natural killer (trNK) cells – broadly defined by markers of tissue-residency, such as CD49a (integrin alpha1, ITGA1) and CD103 (integrin alpha E, ITGAE) – are increasingly recognized for their immunoregulatory role in host control of infection, malignancy, and autoimmunity. Although the importance of transforming growth factor beta (TGFβ) in trNK cell differentiation has been demonstrated, the context in which the differentiation of CD49a+CD103+ trNK cells occurs can result in either an immunosuppressive phenotype or a highly cytotoxic one. To understand this dichotomy better, we utilized a multiomics approach to molecularly characterize these cells and identified a highly cytotoxic trNK (ctrNK) cell phenotype, characterized by the expression of CD39.","dates":{"publication":"2026/05/04"},"accession":"GSE284445","cross_references":{"GSM":["GSM8684433","GSM8684432","GSM8684435","GSM8684434","GSM8684437","GSM8684436","GSM8684438","GSM8684431"],"GPL":["24676"],"GSE":["284445"],"taxon":["Homo sapiens"]}}