B lymphocytes, essential in cellular immunity as antigen-presenting cells and in humoral immunity as major effector cells, play a crucial role in the antitumor response. β-glucan enhanced immunoglobulin (Ig) secretion in previous studies, but the specific mechanisms of B-cell activation with β-glucan were poorly understood. This study demonstrates that β-glucan enhances antitumor immune responses by promoting plasma B cell differentiation via the Dectin-1 receptor. In vitro experiments showed β-glucan enhanced B cell proliferation and differentiation into antibody-secreting plasma cells. In vivo tumor models confirmed that β-glucan treatment significantly improved tumor control through B cell-mediated mechanisms, expanding our understanding of β-glucan's immunomodulatory role beyond innate immunity to include adaptive B cell responses.
This study reveals a novel mechanism by which β-glucan enhances antitumor immunity: through Dectin-1-mediated promotion of B cell differentiation into antibody-secreting plasma cells. Both in vitro and in vivo results confirm that β-glucan activates adaptive humoral immunity, complementing its known effects on innate immune cells (macrophages, NK cells), and providing a mechanistic basis for β-glucan as a cancer immunotherapy adjuvant.
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Bai Y; Ding J; He L; Zhu Z; Pan J; Qi C. β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1. BMC Immunology. 2025. DOI: 10.1186/s12865-025-00681-z. PMID: 39794756.
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