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首页> 外文期刊>Cancer Cell >Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis.
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Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis.

机译：荷瘤宿主中髓样免疫抑制剂Gr + CD11b +细胞的扩增直接促进了肿瘤血管生成。

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摘要

We demonstrate a novel tumor-promoting role of myeloid immune suppressor Gr+CD11b+ cells, which are evident in cancer patients and tumor-bearing animals. These cells constitute approximately 5% of total cells in tumors. Tumors coinjected with Gr+CD11b+ cells exhibited increased vascular density, vascular maturation, and decreased necrosis. These immune cells produce high levels of MMP9. Deletion of MMP9 in these cells completely abolishes their tumor-promoting ability. Gr+CD11b+ cells were also found to directly incorporate into tumor endothelium. Consistent with this observation, Gr+CD11b+ cells acquire endothelial cell (EC) properties in tumor microenvironment and proangiogenic culture conditions. Our data provide evidence that Gr+CD11b+ cells of immune origin induced by tumors directly contribute to tumor growth and vascularization by producing MMP9 and differentiating into ECs.
机译：我们证明了髓样免疫抑制剂Gr + CD11b +细胞的新型肿瘤促进作用，这在癌症患者和荷瘤动物中很明显。这些细胞约占肿瘤总细胞的5％。与Gr + CD11b +细胞共注射的肿瘤表现出增加的血管密度，成熟的血管和减少的坏死。这些免疫细胞产生高水平的MMP9。这些细胞中MMP9的缺失完全消除了它们的促肿瘤能力。还发现Gr + CD11b +细胞直接整合到肿瘤内皮中。与此观察结果一致，Gr + CD11b +细胞在肿瘤微环境和促血管生成培养条件下具有内皮细胞（EC）特性。我们的数据提供了证据，表明由肿瘤诱导的具有免疫原性的Gr + CD11b +细胞通过产生MMP9并分化为EC来直接促进肿瘤生长和血管形成。

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