{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309232/"]},"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=GSE309232"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Matrix viscoelasticity regulates dendritic cell migration and immune priming [ATAC-seq]","description":"The tumor microenvironment shapes immune surveillance through its mechanical properties, yet the role of matrix viscoelasticity remains unclear. Here, we used a collagen system with tunable viscoelasticity to define how matrix relaxation directs dendritic cell (DC) behavior. Elastic matrices impaired DC migration by limiting actomyosin-driven collagen remodeling, thereby reducing DC-T cell encounters and weakening T cell priming, activation, proliferation, and tumor killing. Blocking DC migration in fast-relaxing gels recapitulated key aspects of the impaired T cell priming seen in elastic matrices. Prolonged confinement in elastic ECM induced a mechanomemory state, locking DCs into reduced motility even after transfer to viscoelastic environments, corresponding to altered chromatin accessibility. Finally, studies with patient-derived glioma samples confirmed these findings, identifying viscoelasticity as a barrier to antitumor immunity with implications for therapeutic intervention.","dates":{"publication":"2026/05/13"},"accession":"GSE309232","cross_references":{"GSM":["GSM9263463","GSM9263462","GSM9263461","GSM9263460","GSM9263459","GSM9263458"],"GPL":["34281"],"GSE":["309232"],"taxon":["Homo sapiens"]}}