细胞因子诱导的杀伤细胞
CCR5受体拮抗剂
马拉维洛克
细胞
细胞因子
免疫学
人口
化学
细胞生物学
癌症研究
生物
趋化因子
医学
趋化因子受体
免疫系统
生物化学
CD3型
人类免疫缺陷病毒(HIV)
CD8型
环境卫生
作者
Hong Kyung Lee,Yong Guk Kim,Ji Sung Kim,Eun Jae Park,Boyeong Kim,Ki Hwan Park,Jong Soon Kang,Jin Tae Hong,Youngsoo Kim,Sang‐Bae Han
出处
期刊:Cancer Letters
[Elsevier]
日期:2016-08-01
卷期号:378 (2): 142-149
被引量:18
标识
DOI:10.1016/j.canlet.2016.05.020
摘要
The antitumor activity of cytokine-induced killer (CIK) cells can be increased by co-culturing them with tumor lysate-pulsed dendritic cells (tDCs); this phenomenon has been studied mainly at the population level. Using time-lapse imaging, we examined how CIK cells gather information from tDCs at the single-cell level. tDCs highly expressed CCL5, which bound CCR5 expressed on CIK cells. tDCs strongly induced migration of Ccr5(+/+) CIK cells, but not that of Ccr5(-/-) CIK cells or Ccr5(+/+) CIK cells treated with the CCR5 antagonist Maraviroc. Individual tDCs contacted Ccr5(+/+) CIK cells more frequently and lengthily than with Ccr5(-/-) CIK cells. Consequently, tDCs increased the antitumor activity of Ccr5(+/+) CIK cells in vitro and in vivo, but did not increase that of Ccr5(-/-) CIK cells. Taken together, our data provide insight into the mechanism of CIK cell activation by tDCs at the single-cell level.
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