间充质干细胞
癌症研究
髓源性抑制细胞
CCR2型
肿瘤微环境
间质细胞
生物
骨髓
趋化因子
免疫学
抑制器
趋化因子受体
炎症
细胞生物学
癌症
肿瘤细胞
遗传学
作者
Guangwen Ren,Xin Zhao,Liying Zhang,Zengrong Yuan,Hengqi Zheng,Changshun Shao,Yufang Shi
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2011-04-01
卷期号:186 (1_Supplement): 66.40-66.40
标识
DOI:10.4049/jimmunol.186.supp.66.40
摘要
Abstract Mesenchymal stem cells (MSCs) residing in tumor stroma have been recognized to originate from normal tissues, such as bone marrow. Although they present as a major component of tumor stroma, the exact role they play in tumor progression and how they distinguish from normal tissue MSCs are largely unknown. In this report, we characterized the function of mesenchymal stem cells in promoting tumor development. Compared to BM-MSCs or tissue-MSCs, lymphoma-derived MSCs (L-MSCs) exhibited a strong tumor-promoting effect in a tumor transplantation model. While L-MSCs did not differ from BM-MSCs in their ability to suppress the adaptive immunity, they induced more abundant accumulation of CD11b+Gr-1+ myeloid suppressor cells and F4/80+ macrophages in tumors. Depletion of macrophages, but not myeloid suppressor cells, completely ablated the effect of L-MSCs, indicating that the tumor-promoting effect of L-MSCs was mediated via the recruitment of macrophages. Furthermore, chemokines CCL-2, CCL-7 and CCL-12, all of which utilize CCR2 as a receptor, were found over-expressed in L-MSCs. Correspondingly, the tumor-promoting effect of L-MSCs was largely abolished in CCR2-/- mice. Collectively, these data demonstrated that L-MSCs contribute to tumor development through CCR2-dependent recruitment of macrophages to tumor sites. Our findings thus established a mechanistic link between two major types of tumor stromal cells, providing critical implications for the future cancer therapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI