{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314339/"]},"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=GSE314339"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Early life B cell memory is archived in the mouse B-1 cell compartment and drives Chronic Lymphocytic Leukemia-like disease [scRNA-seq]","description":"The adult B cell pool is a developmental mosaic comprising short-lived naïve B cells and long-lived memory. Using genetic time-stamping, we previously showed that early life origin (ELO) B cells contributed substantially to the adult mouse immune system. In this study, we found that ELO B cells share a memory-like signature. Notably, B-1 cells exhibited an enrichment for the PD-L2/CD80 double positive (DP) immunophenotype associated with highly differentiated memory. Indeed, microbial antigen exposure in neonates expanded distinct specificities within the DP B-1 cell compartment, identifying the latter as a reservoir of IgM memory. B cell chronic lymphocytic leukemia (CLL) is a disease marked by the accumulation of memory-like B cells. By applying time-stamping to a mouse model for unmutated CLL (U-CLL), we demonstrated that leukemic expansion is driven by B-1 cell clones arising prior to postnatal day 10. Importantly, B-1 cells in mice and man closely mirrored the molecular profile of U-CLL. These results suggest that an age-associated leukemia can originate from ELO B cells.","dates":{"publication":"2026/03/09"},"accession":"GSE314339","cross_references":{"GSM":["GSM9393796","GSM9393797"],"GPL":["24247"],"GSE":["314339"],"taxon":["Mus musculus"]}}