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

Yunqiao Li, Raag Bhargava, Jenny Tuyet Tran, Tanya R. Blane, Linghang Peng, Fangkun Luan, Zhe Huang, Zefan Zhang, Yunfan Sun, Changchun Xiao () and David Nemazee ()
Additional contact information
Yunqiao Li: The Scripps Research Institute
Raag Bhargava: The Scripps Research Institute
Jenny Tuyet Tran: The Scripps Research Institute
Tanya R. Blane: The Scripps Research Institute
Linghang Peng: The Scripps Research Institute
Fangkun Luan: The Scripps Research Institute
Zhe Huang: The Scripps Research Institute
Zefan Zhang: Ministry of Education
Yunfan Sun: Ministry of Education
Changchun Xiao: The Scripps Research Institute
David Nemazee: The Scripps Research Institute

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: 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.

Date: 2025
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DOI: 10.1038/s41467-025-59622-4

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