Abstract

Abstract The mechanisms whereby tumors reap the pro-growth benefits of an inflammatory context while still evading the immune response are not fully understood. Using phospho-specific flow cytometry, we demonstrate differential biasing of STAT phosphorylation responses within the tumor microenvironment, with B16 and CT26 cancer cells responding preferentially to pro-inflammatory IL-6 and IFN-γ and tumor-infiltrating T cells responding preferentially to anti-inflammatory IL-10. Investigation of cytokine responsiveness biasing within tumor-infiltrating T cells revealed that the intratumoral T cell population is shaped by non antigen-specific accumulation of CD62L− T cells, which lack responsiveness to pro-inflammatory cytokines despite their robust secretion of these factors. The unchecked production of pro-inflammatory factors by antigen-experienced T cells within the tumor suggests a novel role for these cells in supporting tumor growth by contributing to the inflammatory milieu within the tumor microenvironment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1916.

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