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甲胎蛋白(AFP)复杂的结构决定其在肝癌细胞生长过程中扮演多功能的角色。AFP不仅具有促进肝癌细胞增生的作用,而且还具有抑制肿瘤患者的免疫应答作用。最近研究表明AFP能损伤肝癌患者树突状细胞(DCs)的功能和诱导DCs凋亡;AFP可能通过调节DCs表型分子的表达,抑制DCs转变为成熟的抗原提呈细胞(APC)以及通过影响淋巴细胞或肝癌细胞的肿瘤坏死因子(TNF)家族及其受体的表达,抑制癌细胞内Caspase活性,导致肝癌细胞逃避机体免疫监视。
The complex structure of AFP determines its multifunctional role in the growth of liver cancer cells. AFP not only has the function of promoting the proliferation of hepatoma cells, but also has the effect of inhibiting the immune response of tumor patients. Recent studies have shown that AFP can damage the function of dendritic cells (DCs) and induce apoptosis of DCs in hepatocellular carcinoma patients. AFP may regulate the expression of DCs phenotype molecules, inhibit the conversion of DCs to mature antigen-presenting cells (APCs) Lymphocytes or liver cancer cells tumor necrosis factor (TNF) family and its receptor expression, inhibition of intracellular Caspase activity, leading to liver cancer cells to evade the body immune surveillance.