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首页> 外文期刊>Cancer Cell >Loss of Cutaneous TSLP-Dependent Immune Responses Skews the Balance of Inflammation from Tumor Protective to Tumor Promoting
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Loss of Cutaneous TSLP-Dependent Immune Responses Skews the Balance of Inflammation from Tumor Protective to Tumor Promoting

机译：皮肤依赖TSLP的免疫反应的丧失使从保护肿瘤到促进肿瘤的炎症平衡失调。

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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 β-catenin signaling in the neighboring epithelium. Epithelial specific ablation of β-catenin prevents both carcinogenesis and the accumulation of CD11b +Gr1 + myeloid cells, suggesting tumor cells initiate a feed-forward loop that induces protumorigenic inflammation.
机译：炎症可促进或抑制癌症进展。在这项研究中，我们已经解决了在皮肤癌变过程中促炎细胞因子胸腺基质淋巴细胞生成素（TSLP）的作用。使用分别针对Notch和Wnt信号传导的条件性功能丧失和功能增强小鼠模型，我们证明TSLP介导的炎症通过直接作用于CD4和CD8 T细胞来防止皮肤癌变。 TSLP受体（TSLPR）的遗传消融扰乱了T细胞介导的保护，并导致CD11b + Gr1 +髓样细胞的积累。它们通过分泌Wnt配体并增强邻近上皮细胞的β-catenin信号传导来促进肿瘤生长。 β-catenin的上皮特异性消融可防止癌变和CD11b + Gr1 +骨髓细胞的积聚，这表明肿瘤细胞启动了一个前馈环，诱导了致瘤性炎症。

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