Di Piazza, MatteoNowell, Craig S.Koch, UteDurham, Andre-DanteRadtke, Freddy2013-02-272013-02-272013-02-27201210.1016/j.ccr.2012.08.016https://infoscience.epfl.ch/handle/20.500.14299/89367WOS:000310113900009Inflammation can promote or inhibit cancer progression. In this study we have addressed the role of the proinflammatory cytokine thymic stromal lymphopoietin (TSLP) during skin carcinogenesis. Using conditional loss- and gain-of-function mouse models for Notch and Wnt signaling, respectively, we demonstrate that TSLP-mediated inflammation protects against cutaneous carcinogenesis by acting directly on CD4 and CD8 T cells. Genetic ablation of TSLP receptor (TSLPR) perturbs T-cell-mediated protection and results in the accumulation of CD11b(+)Gr1(+) myeloid cells. These promote tumor growth by secreting Wnt ligands and augmenting beta-catenin signaling in the neighboring epithelium. Epithelial specific ablation of beta-catenin prevents both carcinogenesis and the accumulation of CD11b(+)Gr1(+) myeloid cells, suggesting tumor cells initiate a feed-forward loop that induces protumorigenic inflammation.text::journal::journal article::research article