Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1

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. Our previous work has shown [beta]-glucan enhanced immunoglobulins (Ig) secretion. But the specific mechanisms of B-cell activatio...

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Bibliographic Details
Published in:BMC immunology 2025-01, Vol.26 (1)
Main Authors: Bai, Yu, Ding, Jun, He, Liuyang, Zhu, Zhichao, Pan, Jie, Qi, Chunjian
Format: Article
Language:English
Subjects:
B cells
Cancer
Care and treatment
Cell differentiation
Development and progression
Health aspects
Immune response
Immunotherapy
Oncology, Experimental
Pattern recognition receptors
Physiological aspects
Tumors
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Summary: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. Our previous work has shown [beta]-glucan enhanced immunoglobulins (Ig) secretion. But the specific mechanisms of B-cell activation with [beta]-glucan are poorly understood. Here, we took advantage of [beta]-glucan to improve the antitumor immune response of B cells. In vitro experiments demonstrate that [beta]-glucan enhance the differentiation of B220.sup.lo CD138.sup.+ B cells, up-regulate co-stimulatory molecules, and increase the production of cytokines and Ig in response to various antigens. Using the Dectin-1 knockout mice, we revealed that [beta]-glucan modulate B cell immune responses dependent on Dectin-1 receptor. In mouse models of Lewis lung cancer (LLC) tumors, combining [beta]-glucan with programmed death-1(PD-1) blocking antibodies led to increase recruitment of CD19.sup.+ B cells in the tumor microenvironment (TME), higher numbers of germinal centers B cells (GC B) in the spleen and draining lymph node (DLN), elevate Ig production, and delay tumor progression. These findings reveal that [beta]-glucan can serve as a potent adjuvant to modulate B cell immune responses in a Dectin-1 dependent manner and improve immune checkpoint blockade (ICB) therapy in antitumor.
ISSN:1471-2172
1471-2172
DOI:10.1186/s12865-025-00681-z