人乳头状瘤病毒与喉癌(2)-找论文网

3 HPV感染与喉癌发生、发展的免疫学机制

HPV感染所致喉癌发生、发展是多因素、多步骤的过程，HPV逃避机体的宿主免疫监视，尤其细胞免疫监视也是重要的原因之一。

HPV蛋白的表达与感染细胞的分化状态有密切的关系。在上皮细胞的基底层，有少量mRNA编码病毒E1、E2蛋白，在基底上棘状细胞，E6、E7蛋白在细胞核内有少量表达，在更上层细胞的细胞核和细胞浆E4蛋白和两种病毒衣壳蛋白L1、2有表达，但在数量上有意义的表达仅仅出现在终末期的分化角质细胞（KC），而这种细胞不能分裂增殖，一般1～2天从上皮或粘膜脱落，机体的免疫监视功能不能识别。上皮细胞基底层是最佳的树突状细胞摄取和提呈病毒蛋白的地方，病毒蛋白的表达减少将使机体不能通过免疫效应机制排除有病毒复制细胞。HPV早期蛋白调节局部免疫反应以及喉癌产生的细胞因子所致的免疫抑制和促进肿瘤增殖也是免疫逃逸的机制之一。肿瘤细胞的HLA抗原不表达或表达减少是肿瘤逃逸免疫监控的机制之一［1820］。

综上所述，致瘤型HPV感染是喉癌发生发展的主要原因之一，但仅仅致瘤型HPV感染在很多情况下是不足以引起喉癌，致瘤型HPV感染也可能不是喉癌发生发展的必要条件，机体的遗传特征、免疫状况、癌基因的活化、抑癌基因的失活以及吸烟等因素都有关［21］。

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