Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity

Abstract B cells engage in anti-tumor immunity but how they contribute to cancer suppression remains unclear. We report that inhibiting plasma cell differentiation either in IgMi mice lacking Igh elements needed for antibody secretion or in mice with B cell-specific knockout of Blimp-1 (Blimp-1 BcKO...

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Main Authors: Yunqiao Li, Raag Bhargava, Jenny Tuyet Tran, Tanya R. Blane, Linghang Peng, Fangkun Luan, Zhe Huang, Zefan Zhang, Yunfan Sun, Changchun Xiao, David Nemazee
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59622-4
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author Yunqiao Li
Raag Bhargava
Jenny Tuyet Tran
Tanya R. Blane
Linghang Peng
Fangkun Luan
Zhe Huang
Zefan Zhang
Yunfan Sun
Changchun Xiao
David Nemazee
author_facet Yunqiao Li
Raag Bhargava
Jenny Tuyet Tran
Tanya R. Blane
Linghang Peng
Fangkun Luan
Zhe Huang
Zefan Zhang
Yunfan Sun
Changchun Xiao
David Nemazee
author_sort Yunqiao Li
collection DOAJ
description Abstract B cells engage in anti-tumor immunity but how they contribute to cancer suppression remains unclear. We report that inhibiting plasma cell differentiation either in IgMi mice lacking Igh elements needed for antibody secretion or in mice with B cell-specific knockout of Blimp-1 (Blimp-1 BcKO) promotes rather than inhibits antitumor immunity and increases numbers of activated B cells. Deficiency of Blimp-1 in tumor-infiltrating B cells generates a unique transcription profile associated with expansion of mutated clones targeting cognate tumor cells. Major histocompatibility complex class II (MHC II) is required for anti-tumor efficacy. Blimp-1-deficient B cells have increased expression of CD80 and CD86 costimulatory molecules that enhance effector T cell function. The Blimp-1 inhibitor valproic acid suppresses tumor growth in a B cell-dependent manner. Thus, inhibition of plasma cell differentiation results in enhanced tumor-specific antigen presentation by B cells and thereby tumor repression, suggesting a potential avenue of immunotherapy against cancer.
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publisher Nature Portfolio
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series Nature Communications
spelling doaj-art-9d78a995441d4fa483566fef318807e82025-08-20T01:51:28ZengNature PortfolioNature Communications2041-17232025-05-0116111610.1038/s41467-025-59622-4Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunityYunqiao Li0Raag Bhargava1Jenny Tuyet Tran2Tanya R. Blane3Linghang Peng4Fangkun Luan5Zhe Huang6Zefan Zhang7Yunfan Sun8Changchun Xiao9David Nemazee10Department of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of EducationDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of EducationDepartment of Immunology and Microbiology, The Scripps Research InstituteDepartment of Immunology and Microbiology, The Scripps Research InstituteAbstract B cells engage in anti-tumor immunity but how they contribute to cancer suppression remains unclear. We report that inhibiting plasma cell differentiation either in IgMi mice lacking Igh elements needed for antibody secretion or in mice with B cell-specific knockout of Blimp-1 (Blimp-1 BcKO) promotes rather than inhibits antitumor immunity and increases numbers of activated B cells. Deficiency of Blimp-1 in tumor-infiltrating B cells generates a unique transcription profile associated with expansion of mutated clones targeting cognate tumor cells. Major histocompatibility complex class II (MHC II) is required for anti-tumor efficacy. Blimp-1-deficient B cells have increased expression of CD80 and CD86 costimulatory molecules that enhance effector T cell function. The Blimp-1 inhibitor valproic acid suppresses tumor growth in a B cell-dependent manner. Thus, inhibition of plasma cell differentiation results in enhanced tumor-specific antigen presentation by B cells and thereby tumor repression, suggesting a potential avenue of immunotherapy against cancer.https://doi.org/10.1038/s41467-025-59622-4
spellingShingle Yunqiao Li
Raag Bhargava
Jenny Tuyet Tran
Tanya R. Blane
Linghang Peng
Fangkun Luan
Zhe Huang
Zefan Zhang
Yunfan Sun
Changchun Xiao
David Nemazee
Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
Nature Communications
title Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
title_full Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
title_fullStr Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
title_full_unstemmed Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
title_short Blocking plasma cell fate enhances antigen-specific presentation by B cells to boost anti-tumor immunity
title_sort blocking plasma cell fate enhances antigen specific presentation by b cells to boost anti tumor immunity
url https://doi.org/10.1038/s41467-025-59622-4
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