ArticleImmunotherapy advances2025
Regulatory B cells promote the immunosuppressive microenvironment and progression of clear cell renal cell carcinoma.
Article in Immunotherapy advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Spatial and phenotypic plasticity of B cells in remodeling the tumor microenvironment.Journal for immunotherapy of cancer · 2026Review
- Single-cell transcriptomic landscape of intrahepatic B Cells in MASH.BMC gastroenterology · 2026Article
- Harnessing the duality of regulatory B cells: from identification of characteristic molecules to therapeutic targeting.Immunotherapy advances · 2026Article
- Multi-omics insights into tumor grade progression in clear cell renal cell carcinoma: from molecular mechanisms to precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- The role of ADAM8 in intrahepatic cholangiocarcinoma.Discover oncology · 2025Review
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Authors and funding
10 authors.
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Abstract
Background: Regulatory B cells (Bregs) are critical mediators of immune modulation and tumor progression. However, their prognostic relevance and mechanistic roles in clear cell renal cell carcinoma (ccRCC) remain insufficiently explored. Methods: A comprehensive pancancer strategy was implemented to assess the prognostic role of Breg cells. Spatial transcriptomics, multiplex immunofluorescence (mIF), and immunohistochemistry were performed to investigate Breg localization and immunosuppressive functionality in ccRCC. A machine learning-derived Breg signature (CMLBregS) was established and validated for risk stratification and immune profiling. Results: Elevated Breg signatures were prominently observed in ccRCC and were associated with advanced T stage, higher tumor grades, and decreased progression-free survival. Spatial transcriptomics and mIF revealed that CD20⁺CD23⁺IL10V Breg cells exert immunosuppressive effects, with or without of the presence of tertiary lymphoid structures. The CMLBregS, comprising 16 Breg-related genes, effectively stratified built a binary classification system. A high-CMLBregS score was linked to an immunosuppressive TME characterized by upregulated IL-10 and TGF-β production, suppression of lymphocyte activation, reduced T cell proliferation, and dampened innate immune responses. Patients with higher CMLBregS scores demonstrated significantly worse clinical outcomes across multiple cohorts. Among CMLBregS-related genes, IRF4 emerged as a key prognostic marker, strongly correlating with IL-10 and PDCD1 expression. Notably, patients with elevated CMLBregS scores exhibited poorer responses to immune checkpoint blockade therapy and more aggressive disease progression during immunotherapy. Conclusion: This study underscores the pivotal role of Bregs in promoting immune suppression and poor prognosis in ccRCC. The CMLBregS model offers a robust prognostic tool, identifies patients less likely to benefit from immunotherapy, and highlights IRF4 as a potential alternative target. These findings provide a foundation for future strategies aimed at overcoming Breg-mediated immunosuppression in ccRCC.
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