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

Abstract Background 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 β-glucan enhanced immunoglobulins (Ig) secretion. But the specific mechanisms of B...

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Main Authors: Yu Bai, Jun Ding, Liuyang He, Zhichao Zhu, Jie Pan, Chunjian Qi
Format: Article
Language:English
Published: BMC 2025-01-01
Series:BMC Immunology
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Online Access:https://doi.org/10.1186/s12865-025-00681-z
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author Yu Bai
Jun Ding
Liuyang He
Zhichao Zhu
Jie Pan
Chunjian Qi
author_facet Yu Bai
Jun Ding
Liuyang He
Zhichao Zhu
Jie Pan
Chunjian Qi
author_sort Yu Bai
collection DOAJ
description Abstract Background 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 β-glucan enhanced immunoglobulins (Ig) secretion. But the specific mechanisms of B-cell activation with β-glucan are poorly understood. Here, we took advantage of β-glucan to improve the antitumor immune response of B cells. Results In vitro experiments demonstrate that β-glucan enhance the differentiation of B220lo CD138+ 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 β-glucan modulate B cell immune responses dependent on Dectin-1 receptor. In mouse models of Lewis lung cancer (LLC) tumors, combining β-glucan with programmed death-1(PD-1) blocking antibodies led to increase recruitment of CD19+ 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. Conclusions These findings reveal that β-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. Clinical trial number Not applicable.
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institution Kabale University
issn 1471-2172
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spelling doaj-art-da87a6e502954f0482ccd61abb3add982025-01-12T12:14:03ZengBMCBMC Immunology1471-21722025-01-0126111410.1186/s12865-025-00681-zβ-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1Yu Bai0Jun Ding1Liuyang He2Zhichao Zhu3Jie Pan4Chunjian Qi5Laboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityLaboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityLaboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityLaboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityLaboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityLaboratory of Oncology, Medical Research Center, The Second People’s Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical UniversityAbstract Background 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 β-glucan enhanced immunoglobulins (Ig) secretion. But the specific mechanisms of B-cell activation with β-glucan are poorly understood. Here, we took advantage of β-glucan to improve the antitumor immune response of B cells. Results In vitro experiments demonstrate that β-glucan enhance the differentiation of B220lo CD138+ 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 β-glucan modulate B cell immune responses dependent on Dectin-1 receptor. In mouse models of Lewis lung cancer (LLC) tumors, combining β-glucan with programmed death-1(PD-1) blocking antibodies led to increase recruitment of CD19+ 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. Conclusions These findings reveal that β-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. Clinical trial number Not applicable.https://doi.org/10.1186/s12865-025-00681-zβ-glucanPlasma B cellsDectin-1Tumor immunotherapy
spellingShingle Yu Bai
Jun Ding
Liuyang He
Zhichao Zhu
Jie Pan
Chunjian Qi
β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
BMC Immunology
β-glucan
Plasma B cells
Dectin-1
Tumor immunotherapy
title β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
title_full β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
title_fullStr β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
title_full_unstemmed β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
title_short β-Glucan induced plasma B cells differentiation to enhance antitumor immune responses by Dectin-1
title_sort β glucan induced plasma b cells differentiation to enhance antitumor immune responses by dectin 1
topic β-glucan
Plasma B cells
Dectin-1
Tumor immunotherapy
url https://doi.org/10.1186/s12865-025-00681-z
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