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机构地区:[1]复旦大学附属中山医院皮肤科,上海200032 [2]中国医学科学院皮肤病研究所,南京210042
出 处:《国际免疫学杂志》2014年第3期183-186,共4页International Journal of Immunology
基 金:国家自然科学基金项目(30700727);江苏省自然科学基金项目(2012505);教育部高等学校博士点新教师基金项目(20070023113)
摘 要:在肿瘤微环境内,肿瘤细胞及基质细胞可通过自分泌或旁分泌方式产生趋化因子,与细胞表面相应受体结合可以维持肿瘤细胞生长、促进血管增生、获得转移能力,如CCL2招募巨噬细胞到达肿瘤微环境、CCR7参与肿瘤转移至前哨淋巴结、CXCLl2-CXCR4则与多种肿瘤的转移有关,趋化因子在肿瘤进展中发挥了重要作用。另外,肿瘤细胞还可通过趋化因子募集内皮细胞,抑制免疫监视功能。因而研究肿瘤微环境中与肿瘤生长、转移及免疫逃逸有关的趋化因子及其受体作用机制具有重要意义。Both tumor cells and stromal cells in tumor microenvironment secrete chemokines by autocrine or paraerine mechanisms. These chemokines bind to the chemokine receptors present on the tumor and the stromal cells to sustain tumor cell growth and promote tumor angiogenesis which allows tumor cells to acquire the ability to metastasis. The chemokine receptor CCL2 expression is correlated with macrophage recruitment. CCR7 plays a key role in the migration of tumor cells into the sentinel lymph nodes. CXCL12-CXCR4 axis is involved in the migration of many tumors. Chemokines play a key role in tumor progression. Furthermore, tumor cells could recruit endothelial cells through serected chemokines and impair immune surveillance. In this paper, the role of specific chemokines/chemokine receptor interactions in tumor microenvironment are reviewed in the resoect of tumor orogression, metastasis, evasion of immune surveillance and theraoy to the tumor.
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