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Are tumor-infiltrating macrophages derived from monocyte-lineage belonging to the myeloid-derived suppressor cell?

肿瘤浸润巨噬细胞是否源自属于骨髓源性抑制细胞的单核细胞谱系？

基本信息

批准号：
21590415
负责人：
TAKAMI Tsuyoshi
金额：
$ 3.08万
依托单位：
Gifu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2009
资助国家：
日本
起止时间：
2009 至 2011
项目状态：
已结题

项目摘要

The marker profile, production of cytokine and chemokine, and antigen-presenting capability were studied to clarify the origin of tumor-infiltrating macrophages(TIM). Our results clearly showed that TIM was the hetrogeneous cell population having both capabilities of tumor-suppressing(M1) macrophage and tumor-promoting(M2) macrophages. On the other hand, the treatment of TIM with GM-CSF and siRNA for M-CSF induced the intra-cellular signal transducing molecules such as STAT-1, STAT-5, and STAT-6 of which are necessary for maturation toward antigen-presenting dendritic cells, nevertheless the maker-profiles of treated TIM did not change significantly. However both of the GM-CSF and siRNA for M-CSFR treated and non-treated TIM revealed similar antigen presenting capabilities in the system using OVA-specific TCR transgenic mice. Altogether it was clarified that the phenotype of TIM was reflecting the invading tumor microenvironment, and not certain cell type such as myeloid-derived suppressor cells, but was the cell that still keeped plasticity and could be changed by surrounding microenvironment.

研究了标记谱、细胞因子和趋化因子的产生以及抗原提呈能力，以阐明肿瘤浸润性巨噬细胞（TIM）的起源。我们的结果清楚地表明TIM是具有肿瘤抑制（M1）巨噬细胞和肿瘤促进（M2）巨噬细胞能力的异质细胞群。另一方面，用GM-CSF和M-CSF的siRNA处理TIM诱导了细胞内信号转导分子，如STAT-1、STAT-5和STAT-6，这些分子是抗原呈递树突状细胞成熟所必需的，但处理过的TIM的maker谱并没有显著改变。然而，M-CSFR处理和未处理TIM的GM-CSF和siRNA在ova特异性TCR转基因小鼠的系统中显示出相似的抗原提呈能力。综上所述，TIM的表型反映的是侵袭性肿瘤微环境，而不是髓源性抑制细胞等特定类型的细胞，而是仍保持可塑性，可被周围微环境改变的细胞。