{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306321/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE306321"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell RNA sequencing reveals Lin28b-dependent immune modulation in the PDAC tumor microenvironment","description":"Cancer-associated fibroblasts (CAFs) play a crucial role in shaping the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment (TME). This study investigates the impact of an RNA-binding protein Lin28b on the immune landscape of PDAC. Single-cell RNA sequencing (scRNA-seq) was performed on orthotopic pancreatic tumors from wild-type (WT) and fibroblast-specific Lin28b knockout (Fsp-Cre;Lin28bfl/fl) mice. Our analysis revealed that Lin28b expression in CAFs promotes an immunosuppressive TME characterized by reduced immune cell infiltration and dampened type I interferon (IFN) signaling. Conversely, Lin28b deletion in CAFs resulted in increased infiltration of immune cells, particularly CD8+ T cells and enhanced cytotoxic T cell activity. These findings identify Lin28b as a CAF-intrinsic molecular brake on anti-tumor immunity and provide a rationale for targeting the Lin28 to overcome PDAC resistance to immunotherapy.","dates":{"publication":"2026/06/21"},"accession":"GSE306321","cross_references":{"GSM":["GSM9197382","GSM9197383","GSM9197380","GSM9197381","GSM9197379","GSM9197378"],"GPL":["24247"],"GSE":["306321"],"taxon":["Mus musculus"]}}