<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type> Other</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE293917</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>CTLA-4 blockade enhances germinal center reactions in lymph nodes that drive glioma-specific IgG production and glioma clearance [scRNA/BCR-seq]</name><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.</description><dates><publication>2026/05/28</publication></dates><accession>GSE293917</accession><cross_references><GSM>GSM8893296</GSM><GSM>GSM8893297</GSM><GSM>GSM8893298</GSM><GSM>GSM8893299</GSM><GSM>GSM8893300</GSM><GSM>GSM8893301</GSM><GSM>GSM8893302</GSM><GSM>GSM8893303</GSM><GPL>24247</GPL><GSE>293917</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>