INSERM, U866, Dijon, France.
Trends Mol Med. 2012 Dec;18(12):742-9. doi: 10.1016/j.molmed.2012.09.007. Epub 2012 Oct 17.
The immune system has important roles in limiting the spread of cancer and shaping the tumor microenvironment. Although the contributions of T helper 17 (Th17) cells (a subtype of CD4(+) T lymphocytes) to autoimmunity and allergy response are well known, their roles in cancer remain ambiguous. Despite adoptive transfer studies indicating that mouse Th17 cells support anticancer immunity, the Th17 cells that naturally infiltrate experimental tumors appear to have a tumor-promoting effect. These contradictory properties can be related to the high degree of plasticity inherent in Th17 cells and their capacity to differentiate into tumoricidal Th1-like cells. Mouse Th17 cells induced by transforming growth factor-β (TGF-β) express CD39 and CD73 ectonucleotidases on their surfaces, which leads to adenosine release and suppression of T cell immunity. Here, we discuss how TGF-β acts as a molecular switch controlling the immunoregulatory properties of Th17 cells.
免疫系统在限制癌症的扩散和塑造肿瘤微环境方面起着重要作用。尽管辅助性 T 细胞 17（Th17）细胞（CD4+T 淋巴细胞的一种亚型）在自身免疫和过敏反应中的作用已广为人知，但它们在癌症中的作用仍存在争议。尽管过继转移研究表明，小鼠 Th17 细胞支持抗肿瘤免疫，但自然浸润实验性肿瘤的 Th17 细胞似乎具有促进肿瘤的作用。这些矛盾的特性可以与 Th17 细胞固有的高度可塑性及其分化为杀伤肿瘤的 Th1 样细胞的能力有关。转化生长因子-β（TGF-β）诱导的小鼠 Th17 细胞在其表面表达 CD39 和 CD73 胞外核苷酸酶，导致腺苷的释放和 T 细胞免疫的抑制。在这里，我们讨论了 TGF-β 如何作为一个分子开关控制 Th17 细胞的免疫调节特性。
