| First Author | Di Piazza M | Year | 2012 |
| Journal | Cancer Cell | Volume | 22 |
| Issue | 4 | Pages | 479-93 |
| PubMed ID | 23079658 | Mgi Jnum | J:192029 |
| Mgi Id | MGI:5463833 | Doi | 10.1016/j.ccr.2012.08.016 |
| Citation | Di Piazza M, et al. (2012) Loss of cutaneous TSLP-dependent immune responses skews the balance of inflammation from tumor protective to tumor promoting. Cancer Cell 22(4):479-93 |
| abstractText | Inflammation 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. |
