PDF(Pubmed)
Abstract：
Fibrosis is a common pathophysiological response of many tissues and organs subjected to chronic injury. Despite the diverse aetiology of keloid, lacaziosis and localized scleroderma, the process of fibrosis is present in the pathogenesis of all of these three entities beyond other individual clinical and histological distinct characteristics. Fibrosis was studied in 20 samples each of these three chronic cutaneous inflammatory diseases. An immunohistochemical study was carried out to explore the presence of α-smooth muscle actin (α-SMA) and vimentin cytoskeleton antigens, CD31, CD34, Ki67, p16; CD105, CD163, CD206 and FOXP3 antigens; and the central fibrotic cytokine TGF-β. Higher expression of vimentin in comparison to α-SMA in all three lesion types was found. CD31- and CD34-positive blood vessel endothelial cells were observed throughout the reticular dermis. Ki67 expression was low and almost absent in scleroderma. p16-positive levels were higher than ki67 and observed in reticular dermis of keloidal collagen in keloids, in collagen bundles in scleroderma and in the external layers of the granulomas in lacaziosis. The presence of α-actin positive cells and rarely CD34 positive cells, observed primarily in keloids, may be related to higher p16 antigen expression, a measure of cell senescence. Low FOXP3 expression was observed in all lesion types. CD105-positive cells were mainly found in perivascular tissue in close contact with the adventitia in keloids and scleroderma, while, in lacaziosis, these cells were chiefly observed in conjunction with collagen deposition in the external granuloma layer. We did not find high involvement of CD163 or CD206-positive cells in the fibrotic process. TGF-β was notable only in keloid and lacaziosis lesions. In conclusion, we have suggested vimentin to be the main myofibroblast general marker of the fibrotic process in all three studied diseases, while endothelial-to-mesenchymal transition (EndoMT) and mesenchymal stem cells (MSCs) and M2 macrophages may not play an important role.
摘要：
纤维化是许多组织和器官遭受慢性损伤的常见病理生理反应。尽管瘢痕疙瘩的病因多种多样，拉氮和局限性硬皮病，纤维化过程存在于所有这三个实体的发病机理中，超出了其他个体的临床和组织学特征。在这三种慢性皮肤炎性疾病中的每种20个样品中研究了纤维化。进行了免疫组织化学研究，以探索α-平滑肌肌动蛋白（α-SMA）和波形蛋白细胞骨架抗原的存在，CD31、CD34、Ki67、p16;CD105、CD163、CD206和FOXP3抗原;和中心纤维化细胞因子TGF-β。在所有三种病变类型中，波形蛋白的表达均高于α-SMA。在整个网状真皮中观察到CD31和CD34阳性血管内皮细胞。Ki67在硬皮病中表达低，几乎不存在。p16阳性水平高于ki67，在瘢痕疙瘩的网状真皮中观察到，在硬皮病的胶原束中和拉氏病中肉芽肿的外层中。存在α-肌动蛋白阳性细胞和很少CD34阳性细胞，主要在瘢痕疙瘩中观察到，可能与p16抗原表达增高有关,细胞衰老的测量。在所有病变类型中均观察到低FOXP3表达。CD105阳性细胞主要存在于瘢痕疙瘩和硬皮病血管周围与外膜紧密接触的组织中，while,在拉齐病中，这些细胞主要与胶原蛋白沉积在外部肉芽肿层中一起观察到。我们没有发现CD163或CD206阳性细胞在纤维化过程中的高度参与。TGF-β仅在瘢痕疙瘩和拉齐病中可见。总之,我们建议波形蛋白是所有三种研究疾病中纤维化过程的主要肌成纤维细胞一般标记，而内皮-间质转化（EndoMT）和间充质干细胞（MSCs）和M2巨噬细胞可能不发挥重要作用。
