{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE293nnn/GSE293916/"]},"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=GSE293916"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"CTLA-4 blockade enhances germinal center reactions in lymph nodes that drive glioma-specific IgG production and glioma clearance [bulk RNA-seq]","description":"The orchestration of humoral immunity mediated by B cells in lymph nodes (LNs) is essential for generating adaptive immune response. Despite this crucial role in host defense, B cell responses in cancer have been primarily examined in the tumor microenvironment, while their role in LNs remains largely unexplored. We show that B cell responses in LNs induced by αCTLA-4 regulate glioblastoma (GBM) progression. αCTLA-4 promotes germinal center (GC) formation in deep cervical LNs by enhancing B cell–CD4 T cell interactions, leading to expansion of antigen-specific GC B cells and class switching. This generates tumor-specific IgG, which binds glioma cells and triggers antibody-mediated phagocytosis. Mice lacking antibody-secreting cells fail to benefit from CTLA-4 blockade, underscoring the importance of humoral immunity in tumor control. Our study highlights the role of B cells in tumor-draining LNs and uncovers a novel B cell–dependent mechanism underlying αCTLA-4 efficacy in GBM.","dates":{"publication":"2026/05/28"},"accession":"GSE293916","cross_references":{"GSM":["GSM8893292","GSM8893293","GSM8893294","GSM8893295","GSM8893288","GSM8893289","GSM8893290","GSM8893291"],"GPL":["24247"],"GSE":["293916"],"taxon":["Mus musculus"]}}