Department of Systems Medicine; University of Tor Vergata; Rome, Italy.
Oncoimmunology. 2013 Dec 1;2(12):e26617. doi: 10.4161/onci.26617. Epub 2013 Oct 22.
Immune/inflammatory cells infiltrate almost all human solid tumors and affect all stages of carcinogenesis as they produce different cytokine subsets. The overproduction of T17 cytokines marks the early stages of colorectal carcinoma (CRC) and negatively influences the prognosis of CRC patients. Studies with murine models of CRC have delineated the mechanisms by which T17 cytokines, notably, interleukin (IL)-17A, IL-17F, IL-21, and IL-22, regulate oncogenesis and tumor progression, paving the way to the development of novel anticancer drugs. In this review article, we discuss experimental data supporting the role of T17 cytokines in the modulation of colorectal tumorigenesis.
免疫/炎症细胞几乎浸润所有人类实体瘤,并在产生不同细胞因子亚群时影响癌发生的所有阶段。T17 细胞因子的过度产生标志着结直肠癌 (CRC) 的早期阶段,并对 CRC 患者的预后产生负面影响。CRC 小鼠模型的研究阐明了 T17 细胞因子(特别是白细胞介素 [IL]-17A、IL-17F、IL-21 和 IL-22)调节肿瘤发生和肿瘤进展的机制,为开发新型抗癌药物铺平了道路。在这篇综述文章中,我们讨论了支持 T17 细胞因子在调节结直肠肿瘤发生中的作用的实验数据。