<HashMap><database>GEO</database><scores/><additional><omics_type>Other</omics_type><species>Mus musculus</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315742</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</name><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.</description><dates><publication>2026/05/28</publication></dates><accession>GSE315742</accession><cross_references><GSM>GSM9436131</GSM><GSM>GSM9436132</GSM><GSM>GSM9436123</GSM><GSM>GSM9436124</GSM><GSM>GSM9436125</GSM><GSM>GSM9436126</GSM><GSM>GSM9436127</GSM><GSM>GSM9436128</GSM><GSM>GSM9436129</GSM><GSM>GSM9436130</GSM><GPL>16417</GPL><GSE>315742</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>