关键词：
Immune system
摘要：
B cells in the tumor immune microenvironment (TIME) have garnered significant attention. As a powerful and multifaceted participant in the core network of tumor immunity, B cells exhibit the most diverse effector mechanisms in the tumor microenvironment (TME), such as cytokine secretion and lymphoid organization, antigen presentation and spreading antibody-mediated effector responses, and immunosuppressive regulation. Also similar to other immune cells, the B cell comprises various phenotypes, including both effector and regulatory B cell (Breg) subsets. Notably, Breg plays a key immunosuppressive function in the anti-tumor immune response, making it an indispensable presence in the TME. Importantly, advances in single-cell technologies and spatial transcriptomics have substantially accelerated the characterization of tumor-associated Breg, revealing their tumor-promoting effects in tumors. At present, the characteristic molecules and transcription factors of Breg are unknown. Current definitions rely heavily on functional assays and cytokine profiles, such as interleukin-10 (IL-10), transforming growth factor-β1 (TGF-β1), and interleukin-35 (IL-35), which inhibit the proliferation and cytotoxicity of effector immune cells and induce the generation of regulatory T cell (Treg). Additionally, Breg can suppress anti-tumor immune response through membrane molecules, immunoglobulins, and metabolites. Current studies suggest that Breg is mostly reactive rather than naturally occurring, and both tumor cells and other immune cells can drive Breg differentiation. This reactive differentiation underscores the plasticity of B cells and their adaptability to microenvironmental cues. Studies have further explored the molecular mechanism, suggesting that epigenetic modification and metabolic reprogramming are involved. Furthermore, the clinical implications of Breg are profound. Early studies characterizing elevated Breg infiltration correlate with increased tumor progression, th
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中文科技期刊
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