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• W2910850766 abstract "The immune microenvironment of pancreatic ductal adenocarcinoma (PDA) is comprised of a heterogeneous population of cells that are critical for disease evolution. Prominent among these are the specialized CD1dhiCD5+ regulatory B (Breg) cells that exert a pro-tumorigenic role by promoting tumor cell proliferation. Dissecting the molecular pathways regulating this immune sub-population can thus be valuable for uncovering potential therapeutic targets. Here, we investigate Bruton’s tyrosine kinase (BTK), a key B-cell kinase, as a potential regulator of CD1dhiCD5+ Breg differentiation in the pancreatic tumor microenvironment. Treatment of cytokine-induced B cells in vitro with the high specificity BTK inhibitor Tirabrutinib inhibited CD1dhiCD5+ Breg differentiation and production of IL-10 and IL-35, essential mediators of Breg immunosuppressive functions. The BTK signaling pathway was also found to be active in vivo in PanIN-associated regulatory B cells. Tirabrutinib treatment of mice bearing orthotopic KrasG12D-pancreatic lesions severely compromised stromal accumulation of the CD1dhiCD5+ Breg population. This was accompanied by an increase in stromal CD8+IFNγ+ cytotoxic T cells and significant attenuation of tumor cell proliferation and PanIN growth. Our results uncover a novel role for BTK in regulating CD1dhiCD5+ Breg differentiation and emphasize its potential as a therapeutic target for pancreatic cancer." @default.
• W2910850766 created "2019-01-25" @default.
• W2910850766 creator A5044232696 @default.
• W2910850766 creator A5056698491 @default.
• W2910850766 date "2019-01-11" @default.
• W2910850766 modified "2023-10-17" @default.
• W2910850766 title "BTK signaling drives CD1dhiCD5+ regulatory B-cell differentiation to promote pancreatic carcinogenesis" @default.
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• W2910850766 doi "https://doi.org/10.1038/s41388-018-0668-3" @default.
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