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Immunohistochemical study of psoriatic plaques and perilesional skin in psoriasis vulgaris patients: A pilot study

机译:寻常型银屑病患者银屑病斑块和皮损周围皮肤的免疫组织化学研究:一项初步研究

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摘要

Psoriasis vulgaris, a chronic inflammatory skin disorder, is the result of immune mediated processes, genetic background and environmental factors. Prolactin and the vascular endothelial growth factor seem to play a key role in psoriasis pathogenesis regarding hyperproliferation of epidermal keratinocytes and dermal vascular ectasia. The aim of the study was to investigate the expression of tumor necrosis factor-α (TNF-α), vascular endothelial growth factor receptor 2 (VEGFR2) and prolactin receptor (PRLR) in psoriatic skin by immunohistochemical analysis and to evaluate the correlation with disease severity. Two skin biopsies, psoriatic lesion and perilesional skin, obtained by punch biopsy from 19 nontreated psoriasis patients were examined in hematoxylin and eosin staining and immunohistochemistry (IHC) for TNF-α, VEGFR2 and PRLR. The indirect IHC reaction was carried out automatically and visualized by 3,3-diaminobenzidine (DAB) technique. The average number of DAB-positive cells and the intensity of cell staining were quantified on a predefined scale. The results show a significant difference in the quantity and distribution of TNF-α positive cells in the two sample groups. In psoriatic plaque skin, an increased expression of TNF-α was found in the perivascular dermis and epidermic keratinocytes. In perilesional skin the immunostaining was predominant in the basal layer keratinocytes, while in psoriatic plaque, all the layers were positively marked, with stronger expression at the base. A statistically significant difference was found between the intensity of the immunostaining in the two types of tissue. Positive cells for VEGFR2 and PRL were identified in the basal layer keratinocyte cells (VEGFR2), sweat glands and hair outer shaft sheath (PRLR), without significant differences between the two types of samples. Our findings confirm the importance of TNF-α in psoriasis pathogenesis and a positive correlation with lesions severity. No significant differences were found for VEGFR2 and PRLR, but additional studies are necessary to establish their role.
机译:寻常型牛皮癣是一种慢性炎症性皮肤病,是免疫介导过程,遗传背景和环境因素的结果。催乳素和血管内皮生长因子似乎在银屑病发病机理中起着关键作用,涉及表皮角质形成细胞过度增生和皮肤血管扩张。该研究的目的是通过免疫组织化学分析银屑病皮肤中肿瘤坏死因子-α(TNF-α),血管内皮生长因子受体2(VEGFR2)和催乳素受体(PRLR)的表达,并评估其与疾病的相关性。严重性。在苏木精和曙红染色以及免疫组化(IHC)中检查了从19名未经治疗的牛皮癣患者中通过穿孔活检获得的两种皮肤活检,即银屑病皮损和周围皮损,并进行了TNF-α,VEGFR2和PRLR的检查。间接的IHC反应自动进行,并通过3,3-二氨基联苯胺(DAB)技术进行可视化。 DAB阳性细胞的平均数量和细胞染色的强度以预定的比例进行量化。结果表明,在两个样品组中,TNF-α阳性细胞的数量和分布存在显着差异。在牛皮癣菌斑皮肤中,在血管周真皮和表皮角质形成细胞中发现TNF-α表达增加。在病灶周围皮肤中,免疫染色在基底层角质形成细胞中占主导地位,而在牛皮癣菌斑中,所有层均被阳性标记,在基底处表达更强。在两种类型的组织中,免疫染色强度之间存在统计学上的显着差异。在基底层角质形成细胞(VEGFR2),汗腺和毛发干轴鞘(PRLR)中鉴定出VEGFR2和PRL阳性细胞,两种类型的样品之间无显着差异。我们的发现证实了TNF-α在牛皮癣发病机理中的重要性,并与病灶的严重程度呈正相关。没有发现VEGFR2和PRLR有显着差异,但是需要进一步的研究来确定它们的作用。

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