{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320248/"]},"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=GSE320248"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell sequencing study of splenocytes and YFP+ B cells to investigate differences between Eif3e cg1cre knockout mice and control mice","description":"To gain insights into the cellular mechanisms underlying the lymphoproliferative disorder developed in cKO mice, we performed single cell RNA-seq (scRNA-seq) analysis of YFP+ and total splenocytes from cKO and control mice at the age of 2 months, when lymphocyte activation and proliferation had not yet become obvious.Through our study, we found that Eif3e-deficient B cells are impaired in their development into GCB and PC, becoming blocked at the pre-GCB stage. Additionally, all B cells exhibited high expression of MHC-II. Among CD4+ T cells, the TFH cell population was significantly expanded in cKO mice and showed high expression of IL4. Based on the early-stage phenotype of this mouse model, we hypothesize that Eif3e-deficient B cells promote IL4 expression in CD4+ T cells, which in turn stimulates upregulation of MHC-II on all B cells. The increased MHC-II further enhances CD4+ T cell activation, forming a positive feedback loop.","dates":{"publication":"2026/05/01"},"accession":"GSE320248","cross_references":{"GSM":["GSM9538337","GSM9538336","GSM9538339","GSM9538338","GSM9538335","GSM9538334","GSM9538340","GSM9538341"],"GPL":["24247"],"GSE":["320248"],"taxon":["Mus musculus"]}}