The interaction of tumor cells and myeloid-derived suppressor cells in chronic myelogenous leukemia

被引:9
|
作者
Xu, Hui [1 ,2 ]
Liu, Jingjing [3 ]
Shen, Na [4 ]
Zhao, Zhe [5 ]
Cui, Jieke [6 ]
Zhou, Shu [4 ]
Jiang, Lin [4 ]
Zhu, Xiaoying [4 ]
Tang, Ling [4 ]
Liang, Haitao [4 ]
Liu, Wen [4 ]
Zhu, Zunmin [2 ,7 ]
Meng, Li [8 ]
Zhu, Xiaojian [8 ]
机构
[1] Jinzhou Med Univ, Postgrad Coll, Jinzhou, Liaoning, Peoples R China
[2] Henan Prov Peoples Hosp, Inst Hematol, Zhengzhou 450003, Henan, Peoples R China
[3] Henan Univ Sci & Technol, Affiliated Hosp 1, Dept Hematol, Luoyang, Peoples R China
[4] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Hematol, Wuhan, Hubei, Peoples R China
[5] Hubei Univ Nationalities, Dept Hematol, Minda Hosp, Enshi 445000, Hubei, Peoples R China
[6] Zhengzhou Univ, Affiliated Hosp 1, Dept Hematol, Zhengzhou, Henan, Peoples R China
[7] Henan Prov Peoples Hosp, Sci & Technol Dept Henan Prov, Key Lab Stem Cell Regulat & Differentiat, Zhengzhou, Henan, Peoples R China
[8] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Hematol, Wuhan, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Chronic myelogenous leukemia (CML); myeloid-derived suppressor cells (MDSCs); microvesicles (MVs); treatment-free remission (TFR); MOLECULAR RESPONSE; IMATINIB; MICROENVIRONMENT; MICROVESICLES; DISCONTINUATION; DASATINIB; MONOCYTES; EXOSOMES; LIFE;
D O I
10.1080/10428194.2019.1658098
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Myeloid-derived suppressor cells (MDSCs) are considered to be a strong contributor to the immunosuppressive tumor microenvironment. In our study, the counts of MDSCs were correlated with the remission status of CML patients, especially the M-MDSCs. M-MDSCs promoted the proliferation of K562 cells or CD34+ cells from newly diagnosed CML patients, no matter in cells or mice experiments. We also established a TKI discontinuation model using the K562 cell line for examining the effect of microvesicles (MVs) derived from K562 cells before and after TKI discontinuation on MDSCs. We found a mutual promotion of proliferation of tumor cells and MDSCs. Moreover, MVs derived from K562 cells after TKI discontinuation significantly improved the proliferation of MDSCs compared with MVs from before TKI discontinuation. The bidirectional interaction results in a vicious cycle, by providing a protective niche against immune attacks. Therapeutic interventions modulating this interaction might accelerate the success of TFR.
引用
收藏
页码:128 / 137
页数:10
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