{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338652/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338652"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional profiling of mice decidual CX3CR1+ and CX3CR1- primed CD8 T cells","description":"Deciphering the immune privilege of maternal-fetal interface is critical to understand how reproductive success and host defense are simultaneously maintained. Here, we identify a conserved subset of effector-like memory CD8⁺ T cells that are preferentially infiltrate in the decidua of both humans and mice, via the CX3CL1–CX3CR1 axis. Murine decidual CX3CR1⁺ memory CD8⁺ T cells and human decidual CX3CR1⁺ CD8⁺ T cells share transcriptional and functional programs, characterized by reduced cytokine output but enhanced cytotoxic granule production. We show that decidual stromal cells upregulate CX3CL1 during decidualization, which recruits CX3CR1⁺ cells via receptor engagement and internalization. Functionally, these cells mediate enhanced local protection against Listeria monocytogenes infection at the fetal-maternal interface in a CX3CL1-dependent manner, without contributing to fetal damage. These findings define a conserved mechanism by which decidual tissues selectively enrich effector-like memory CD8⁺ T cells, enabling localized pathogen surveillance while maintaining maternal–fetal tolerance.","dates":{"publication":"2026/09/30"},"accession":"GSE338652","cross_references":{"GSM":["GSM9879139","GSM9879138","GSM9879135","GSM9879134","GSM9879137","GSM9879136"],"GPL":["24247"],"GSE":["338652"],"taxon":["Mus musculus"]}}