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目的通过窄谱中波紫外线(NB-UVB)照射诱发小鼠皮肤肿瘤,探讨Fas/FasL,CD4及CD8在Bowen病(BD)、光老化皮肤及正常小鼠皮肤中的表达情况,加深对皮肤肿瘤Fas/FasL凋亡途径和免疫逃逸机制及周围浸润淋巴细胞类型的认识。方法将42只健康的昆明种小鼠分为两组,慢性照光组(UVB)32只,正常组10只。应用免疫组化法检测其Fas/FasL,CD4及CD8的表达情况。结果成功制作了NB-UVB致小鼠皮肤癌模型。Fas表达光老化皮肤组高于正常鼠皮肤,BD组低于光老化组,FasL表达BD组和光老化组均高于正常鼠皮肤,BD组较光老化组增高,CD4在BD组较正常鼠皮肤及光老化皮肤组均降低,光老化组较正常鼠增高,CD8在BD组、光老化组较正常鼠增高,差异均有统计学意义(P均<0.05),而BD组和光老化组间差异无统计学意义(P>0.05)。结论 FasL在光老化皮肤中表达增高,在BD中进一步增高,支持了Fas/FasL系统启动细胞凋亡过程和肿瘤细胞通过表达FasL来逃避机体免疫监视的学说。BD组与正常皮肤组相比,CD4表达降低,CD8表达增高,这可能与BD是表皮内鳞状细胞癌且存在向侵袭性癌转变的倾向有关。
Objective To investigate the expression of Fas / FasL, CD4 and CD8 in Bowen’s disease (BD), photoaging skin and normal mouse skin by NB-UVB irradiation, Awareness of Tumor Fas / FasL Apoptosis Pathway, Immune Escape Mechanism and Peripheral Infiltrating Lymphocyte Types. Methods Forty-two healthy Kunming mice were divided into two groups: 32 in the chronic light group (UVB) and 10 in the normal group. Immunohistochemistry was used to detect the expression of Fas / FasL, CD4 and CD8. Results NB-UVB induced mouse skin cancer model was successfully established. The expression of Fas in the light-aged skin group was higher than that in the normal mouse skin group, the BD group was lower than the light aging group, the expression of FasL in BD group and the photoaging group were higher than those in the normal mouse skin group, BD group was higher than the photoaging group, (P <0.05), but there was a significant difference between BD group and photoaging group (P <0.05). There was a significant difference between BD group and photoaging group No statistical significance (P> 0.05). Conclusion The expression of FasL in photo-aged skin is increased and further increased in BD, which supports the theory that Fas / FasL system initiates apoptosis and tumor cells escape the immune surveillance by expressing FasL. Compared with normal skin group, BD decreased the expression of CD4 and increased the expression of CD8 in BD group, which may be related to the tendency of BD to be squamous cell carcinoma in epidermis and to metastasis to invasive carcinoma.