IL-17A produced by peritoneal macrophages promote the accumulation and function of granulocytic myeloid-derived suppressor cells in the development of colitis-associated cancer
IL-17A produced by peritoneal macrophages promote the accumulation and function of granulocytic myeloid-derived suppressor cells in the development of colitis-associated cancer
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腹膜巨噬细胞产生的 IL-17A 促进粒细胞骨髓源性抑制细胞在结肠炎相关癌症发展中的积累和功能
DOI：
10.1007/s13277-016-5414-2
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发表时间：
2016-12
期刊：
影响因子：
--
通讯作者：
Wang Shengjun
中科院分区：
文献类型：
--
作者：
Zhang Yue;Wang Juan;Wang Wenxin;Tian Jie;Yin Kai;Tang Xinyi;Ma Jie;Xu Huaxi;Wang Shengjun
人们普遍认为炎症和结肠癌之间有密切的关系。白细胞介素（IL）-17 A和骨髓源性抑制细胞（MDSC）在结肠炎相关癌（CAC）的发生发展中起重要作用。然而，在结直肠慢性炎症依赖性肿瘤中尚未观察到CAC进展期间IL-17、MDSC和Th 17细胞的精确变化。在本研究中，我们发现IL-17在CAC模型的早期在致病结肠部位的水平升高。进一步的实验表明，当暴露于葡聚糖硫酸钠（DSS）时，腹腔巨噬细胞分泌的IL-17可能增加。在体外，我们发现IL-17可以增强粒细胞（G）-MDSC的存活和抑制功能，与炎症相关的子集。随着CAC的发展，巨噬细胞分泌大量IL-17，MDSCs和Th 17细胞的比例不断增加。MDSCs的增殖早于Th 17细胞，且增殖快于Th 17细胞。选择性去除MDSCs不仅减缓CAC过程，而且显著减少体内Th 17细胞。此后，我们证实在CAC的发生发展过程中，腹腔巨噬细胞分泌的IL-17可以促进G-MDSCs的聚集，进而增加Th 17细胞的比例，最终促进CAC的发生发展。
It is widely acknowledged that a close relationship is between inflammation and colon cancer. Interleukin (IL)-17A and myeloid-derived suppressor cells (MDSCs) play an important role in the development of colitis-associated cancer (CAC). However, the precise changes of IL-17, MDSCs, and Th17 cells during the CAC progression have not been observed in the colorectal chronic inflammation-dependent tumor. In this study, we found the level of IL-17 was increased in pathogenic colon site during the early stage of CAC model. Further experiments showed the increased IL-17 was probably secreted by peritoneal macrophages when exposed to dextran sulfate sodium (DSS). In vitro, we found that IL-17 could enhance survival and suppressive function of granulocytic (G)-MDSCs, the subset associated with inflammation. With the development of CAC, the proportions of MDSCs and Th17 cells were continuously increased by the high level of IL-17 produced by macrophages. However, the increase of MDSCs was earlier and acuter than that of Th17 cells. Selective depletion of MDSCs not only slowed down CAC process but also significantly reduce Th17 cells in vivo. Thereafter, we demonstrated that in the development of CAC, IL-17 secreted by peritoneal macrophages could promote the accumulation of G-MDSCs, then the proportion of Th17 cells was increased, and finally promote the development of CAC.
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