{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308872/"]},"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=GSE308872"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"ILC2 regulate a fibroblast progenitor niche in the pancreas (Dpp4CreERT2 lineage trace scRNA-seq)","description":"Local fibroblast development and densities greatly influence organ health and disease, although it remains unclear how tissue fibroblast topography is controlled in situ. Here we define group 2 innate lymphoid cells (ILC2) as key regulators of fibroblast homeostasis in the pancreas. ILC2 co-localise with Pi16+Dpp4+Ly6c+ fibroblasts in an interstitial niche of the exocrine pancreas, which encapsulates the organ parenchyma. ILC2 specifically regulate the expansion of Pi16+Dpp4+Ly6c+ fibroblasts, which have progenitor capacity, while paradoxically also restraining differentiated intra-parenchymal Col15a1+ fibroblasts during inflammation. These homeostatic circuits reinforce fibroblast numbers after injury and set an inflammatory threshold. The ILC2-Pi16+Dpp4+Ly6c+ fibroblast progenitor niche expands locally in cancer, and controls cancer associated fibroblast ontogeny and density. Hence, ILC2-fibroblast dialogue represents a regulatory node that locally orchestrates tissue homeostasis and pathology.","dates":{"publication":"2026/07/03"},"accession":"GSE308872","cross_references":{"GSM":["GSM9254817","GSM9254818"],"GPL":["34328"],"GSE":["308872"],"taxon":["Mus musculus"]}}