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CTLA-4 blockade enhances germinal center reactions in lymph nodes that drive glioma-specific IgG production and glioma clearance [scRNA/BCR-seq]

GSE293917 Mus musculus Expression profiling by high throughput sequencing; Other 8 samples Submitted 2026/05/28 Platform GPL24247
Summary
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.
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Also filed as BioProject PRJNA1247423 and SRA study SRP576843. Searching any of these in the dataset finder brings you back here.

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