{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315742/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Mus musculus"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315742"],"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","description":"Humoral immunity, which is mediated by B cells that mature in germinal centers (GCs) in lymph nodes (LNs), is essential for adaptive immune responses. However, the involvement of B cell responses in anti-tumor and immunotherapy responses remains largely unexplored. Here, we show that activation of B cells in GCs of tumor-draining deep cervical LNs (dcLNs) is necessary for the efficacy of CTLA-4 immune checkpoint blockade in glioma in vivo. We demonstrate that anti-CTLA-4 therapy enhances follicular helper T cell (Tfh) expansion in dcLNs, leading to GC B cell formation, class switching to IgG, and the generation of glioma-specific antibodies. Glioma-bearing mice lacking antibody-secreting cells did not benefit from CTLA-4 blockade. Furthermore, using our new in vivo reporter system, we show that distally-secreted glioma-specific IgG infiltrates the tumor microenvironment and triggers glioma cell phagocytosis. Our study uncovers a previously unknown B cell–dependent mechanism underlying anti-CTLA-4 mediated control of glioma, which could be harnessed to treat other tumor types.","dates":{"publication":"2026/05/28"},"accession":"GSE315742","cross_references":{"GSM":["GSM9436131","GSM9436132","GSM9436123","GSM9436124","GSM9436125","GSM9436126","GSM9436127","GSM9436128","GSM9436129","GSM9436130"],"GPL":["16417"],"GSE":["315742"],"taxon":["Mus musculus"]}}