Fas、FasL表达在银屑病发病机理中的作用

Apoptosis Induced by Fas, FasL in the Pathogenesis of Psoriasis

目的探讨Fas、FasL介导的细胞凋亡引发的免疫调节在银屑病发病机理中的作用及意义。方法采用免疫组化方法和原位末端标记方法研究银屑病患者不同期皮损中Fas、FasL表达与细胞凋亡、局部单一核细胞浸润程度之间的关系。结果①角质形成细胞既可表达Fas,又可表达FasL ,二者分布基本一致 ;Fas、FasL表达强的部位角质形成细胞凋亡明显 ,而局部单一核细胞浸润减少。②患者进行期斑块型皮损中Fas、FasL表达低于相邻非皮损区及恢复期皮损 ,正常表皮基本不表达。结论银屑病皮损中角质形成细胞与单一核细胞间不能有效地借助于Fas系统进行免疫杀伤和免疫调节从而参与该病的发生。

Objective To study the relationship between Fas,FasL and apoptosis and their roles in the pathogenesis of psoriasis. Methods Immunohistochemical techniques were employed to study the expression of Fas,FasL in the uninvolved skin, progressive plaque lesions and regressive lesions. Apoptosis was detected with terminal deoxynucleotidyl transferase mediated dUTP DIG nick end labeling (TUNEL). Results ①Both Fas and FasL were expressed on the keratinocytes with basically the same distribution. There were obvious apoptosis of keratinocytes but reduced infiltration of mononuclear cells (MNCs) in the epidermis with intensive Fas and FasL staining. ②There was a significantly upregulated expression of Fas,FasL in uninvolved skin adjacent to the lesions and regressive lesions compared with that in progressive plaque lesions, as well as in normal skin. Conclusion The downregulated expression of Fas and FasL and increased infiltration of MNCs might contribute to ineffective immunosurveillance and immunoregulation in psoriatic lesions, which might be involved in the pathogenesis of psoriasis.