BTK signaling drives CD1d^hiCD5⁺ regulatory B-cell differentiation to promote pancreatic carcinogenesis.

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 CD1d^hiCD5⁺ regulatory B (B_reg) 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 CD1d^hiCD5⁺ B_reg differentiation in the pancreatic tumor microenvironment. Treatment of cytokine-induced B cells in vitro with the high specificity BTK inhibitor Tirabrutinib inhi

SUBMITTER: Das S 

PROVIDER: S-EPMC6486434 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature