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- W4313366275 abstract "Abstract The host immune response can be corrupted by cancer cells during tumor progression. Here we showed that B lymphocytes played an important role in promoting murine breast cancer (BCa) development, as B cell-deficient mMT mice displayed virtually abrogated tumor growth from transplanted syngeneic ERa+ breast adenocarcinoma cells, concomitant with reduced PD-L1 expression and increased BCa cell death. In murine BCa tumors and tumor-associated lymph nodes, B cells were the major source of IL-27, a pleotropic cytokine with both pro- and anti-inflammatory functions. Deficiency in IL-27 expression specifically in B cells abolished the BCa tumor growth, showing that the effect of B cells in BCa development was mainly through IL-27 production, as likely induced by TLR ligands in the tumor microenvironment together with CD154 and IL-21 expressed by tumor-infiltrating CD4+ T cells. IL-27 treatment of BCa cells resulted in STAT1 and STAT3 phosphorylation, upregulated PD-L1 gene expression and enhanced cell growth. In addition, IL-27 induced activated B cells to express PD-L1 in vitro, consistent with high levels of PD-L1 expression by B cells in tumors. In humans, IL-27 receptor genes were highly expressed in the breast tissue, at levels comparable to those in lymphoid organs, and high IL-27 gene expression was associated with reduced survival in BCa patients, who displayed increased circulating IL-27 levels. Finally, IL-27 supported human BCa cell growth in the presence of tamoxifen, suggesting a role of IL-27 in the drug resistance. Thus, TLR-fueled IL-27 induction in B cells reinforces PD-L1 expression in the tumor environment to drive BCa cell growth and to promote generation of PD-L1hi B regulatory cells, leading to BCa tumor progression." @default.
- W4313366275 created "2023-01-06" @default.
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- W4313366275 date "2019-05-01" @default.
- W4313366275 modified "2023-10-16" @default.
- W4313366275 title "B cells produce IL-27 to upregulate PD-L1 expression and promote breast cancer development" @default.
- W4313366275 doi "https://doi.org/10.4049/jimmunol.202.supp.195.6" @default.
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