摘要
引言机体发生肿瘤时,肿瘤细胞可以凭借多种方式逃避免疫系统的监控、攻击而继续分裂生长,即肿瘤的免疫逃逸。本文围绕肿瘤细胞免疫过程中肿瘤抗原表达、抗原识别、加工、提呈、T细胞增殖、活化和分化以及免疫效应的产生这一系列环节,就近年来肿瘤免疫逃逸机制的有关研究进展作一综述。1 抗原提呈细胞的抗原识别加工提呈障碍1.1 树突状细胞的凋亡及抗原递呈能力的下降树突状细胞(Dendriticcell,DC)在抗原的捕获、加工、提呈和激活淋巴细胞产生免疫反应中起着相当重要的作用[1] ,肿瘤患者的树突状细胞功能常存在缺陷。在对鼠肿瘤细胞系B16、MCA2 0 7、MCA10 2的研究中发现,其细胞培养悬液中C16和C2 4酰基鞘氨醇明显升高,并且可诱导骨源性DC凋亡,给予酰基鞘氨醇合成酶抑制剂降低内源性酰基鞘氨醇水平可避免肿瘤细胞诱导的DC凋亡,而其他的DC保护因子如:脂多糖(LPS)、肿瘤坏死因子α(TNF alpha)此时对DC凋亡无保护作用。进一步研究发现如先给予磷酸肌醇 3 激酶抑制剂预处理,则酰基鞘氨醇合成酶抑制剂对肿瘤细胞诱导的DC凋亡的保护作用将消失,由此认为酰基鞘氨醇通过下调PI3K途径实现肿瘤细胞诱导的D...
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