背景:硬化性苔藓(LiS)是一种慢性硬化萎缩性疾病,通常会影响肛门生殖器区域,有时会影响生殖器外部位。CD34阳性真皮树突状细胞(DDC)有助于维持真皮微结构和调节免疫应答。p53是重要调控细胞周期和凋亡的抑癌基因。类似于硬叶(与LiS密切相关的硬化状况),真皮硬化,DDC的改变,真皮微脉管系统可能是LiS的重要潜在致病机制。
目的:为了检查CD34阳性DDCs的概况,微血管密度(MVD),和p53蛋白在LiS中。
方法:DDC的免疫组织学特征,MVD,在19例LiS及其年龄和性别匹配的正常皮肤(10个标本)中检查了p53,使用抗CD34和p53的抗体。
结果:与正常皮肤中CD34阳性DDCs的丰度相比,LiS中的CD34阳性DDCs的计数明显减少(1.7±0.5/mm2)或完全丧失(23.4±2.1/mm2,p=0.000)。与正常皮肤(5.50±0.20,p=0.000)相比,LiS病变(20±0.47)的MVD显着增加。在正常皮肤和LiS病变的表皮基底细胞角质形成细胞中观察到不连续的单细胞p53弱阳性核染色。
结论:据作者所知,这是第一项分析DDC的研究,MVD,和p53一起在LiS中。研究结果表明,DDC和MVD的改变在LiS的发病机理中起作用。
BACKGROUND: Lichen sclerosus (LiS) is a chronic scleroatrophic condition that usually affects the anogenital area and occasionally the extragenital sites. CD34-positive dermal dendritic cells (DDCs) contribute to the maintenance of the dermal microarchitecture and modulation of the immune response. p53 is a tumor suppressor gene important for the regulation of the cell cycle and apoptosis. Similar to morphea (a LiS-closely related scleroatrophic condition), dermal sclerosis, alterations of DDCs, and dermal microvasculature may be important underlying pathogenetic mechanisms in LiS.
OBJECTIVE: To examine the profile of CD34-positive DDCs, microvessel density (MVD), and p53 protein in LiS.
METHODS: The immunohistological profiles of DDCs, MVD, and p53 were examined in 19 cases of LiS and their age- and sex-matched normal skin (10 specimens), using antibodies against CD34 and p53.
RESULTS: There was a markedly decreased counts (1.7 ± 0.5/mm2) or complete loss of CD34-positive DDCs in LiS against their abundance in the normal skin (23.4 ± 2.1/mm2, p = 0.000). MVD was markedly increased in LiS lesions (20 ± 0.47) as compared to normal skin (5.50 ± 0.20, p = 0.000). Discontinuous single-cell p53 weakly positive nuclear staining was seen in the epidermal basal cell keratinocytes in normal skin and LiS lesions.
CONCLUSIONS: To the best of this author\'s knowledge, this is the first study analyzing DDCs, MVD, and p53 profiles together in LiS. The findings suggest that alterations of DDCs and MVD have roles in the pathogenesis of LiS.