Granata Mariagrazia, Skarmoutsou Evangelia, Mazzarino Maria Clorinda, D'Amico Fabio
Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Methods Mol Biol. 2019;1929:729-738. doi: 10.1007/978-1-4939-9030-6_45.
Psoriasis, an inflammatory autoimmune skin disease, is the result of a chronic interaction between hyperproliferative keratinocytes and infiltrating activated immune cells. The mechanisms underlying psoriasis pathogenesis remain largely unknown, although a combination of genetic and environmental factors plays an important role in its development. S100A7 is overexpressed in psoriasis, and there is growing evidence that S100A7 may be involved in the pathogenesis of psoriasis. Since the mechanisms underlying S100A7 regulation and function remain elusive, a better understanding of these mechanisms may be useful to uncover additional treatment approaches for psoriasis. Immunohistology provides invaluable tools for a better understanding of the pathogenetic mechanisms of psoriasis. Here, we describe basic methods for immunofluorescence and immunohistochemistry analysis of S100A7 expression in psoriatic patients as well as in S100A7 CRISPR-activated human keratinocyte cell line.
银屑病是一种炎症性自身免疫性皮肤病,是过度增殖的角质形成细胞与浸润的活化免疫细胞之间长期相互作用的结果。尽管遗传和环境因素的综合作用在银屑病的发生发展中起着重要作用,但其发病机制在很大程度上仍不清楚。S100A7在银屑病中过度表达,越来越多的证据表明S100A7可能参与银屑病的发病机制。由于S100A7调控和功能的机制仍不清楚,更好地了解这些机制可能有助于发现银屑病的其他治疗方法。免疫组织学为更好地理解银屑病的发病机制提供了宝贵的工具。在这里,我们描述了在银屑病患者以及S100A7 CRISPR激活的人角质形成细胞系中对S100A7表达进行免疫荧光和免疫组织化学分析的基本方法。