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- W2002157461 abstract "TGF-beta blockade significantly slows tumor growth through many mechanisms, including activation of CD8(+) T cells and macrophages. Here, we show that TGF-beta blockade also increases neutrophil-attracting chemokines, resulting in an influx of CD11b(+)/Ly6G(+) tumor-associated neutrophils (TANs) that are hypersegmented, more cytotoxic to tumor cells, and express higher levels of proinflammatory cytokines. Accordingly, following TGF-beta blockade, depletion of these neutrophils significantly blunts antitumor effects of treatment and reduces CD8(+) T cell activation. In contrast, in control tumors, neutrophil depletion decreases tumor growth and results in more activated CD8(+) T cells intratumorally. Together, these data suggest that TGF-beta within the tumor microenvironment induces a population of TAN with a protumor phenotype. TGF-beta blockade results in the recruitment and activation of TANs with an antitumor phenotype." @default.
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- W2002157461 date "2009-09-01" @default.
- W2002157461 modified "2023-10-14" @default.
- W2002157461 title "Polarization of Tumor-Associated Neutrophil Phenotype by TGF-β: “N1” versus “N2” TAN" @default.
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- W2002157461 doi "https://doi.org/10.1016/j.ccr.2009.06.017" @default.
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