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作 者:王玮[1] 周艳宏 李夏雨[1,3] 沈守荣[1,3]
机构地区:[1]中南大学湘雅三医院消化内科,长沙410013 [2]肿瘤研究所,长沙410078 [3]湖南省非可控性炎症与肿瘤重点实验室,长沙410078
出 处:《中南大学学报(医学版)》2012年第6期637-641,共5页Journal of Central South University :Medical Science
基 金:国家自然科学基金(81172300);湖南省博士生科研创新项目(71131110015);中南大学2011年度米塔尔学生创新创业项目(11MX25)~~
摘 要:溃疡性结肠炎是病因不明的肠道非特异性炎症,其癌变风险呈逐年上升的趋势。巨噬细胞是机体免疫系统的重要组成,在炎症时发挥积极的免疫作用;但在肿瘤微环境中出现表型及功能的改变,其释放的大量细胞因子作用于结肠癌细胞,能促进结肠癌细胞增殖、抑制其凋亡、促进血管生成等。受肿瘤影响的巨噬细胞,还通过与其他炎症细胞相互作用,改变机体的免疫功能,形成免疫抑制。故巨噬细胞的改变与溃疡性结肠炎癌变的过程密不可分。Ulcerative colitis is a non-specific colorectal inflammation of unknown causes. It is now known to complicate the dangers of colorectal cancer more than was previously thought. Macrophages are an important part of immune system and play a positive role in immune reaction. But it has been shown that the phenotype and the function of macrophages change in the tumor microenvironment. q-hrough their interaction with colorectal cancer cells and by releasing large quantities of cytokines, macrophages promote colorectal cancer cells by inhibiting angiogenesis and inhibit apoptosis. But the macrophages are also affected by cancer, interact with other inflammatory ceils, and become immune suppressed. Thus the changes of macrophages are inseparable with colitis-associated colorectal carcinogenesis.
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