【佳学基因检测】IL-1 受体敲除小鼠在暴露于 UVB 辐射后出现表皮囊肿并表现出改变的先天免疫反应

基因检测价格表全面吗？

在高峰论坛中肿瘤基因检测及基因突变的改进与提高获悉《J Invest Dermatol》在. 2017 Nov;137(11):2417-2426.发表了一篇题目为《IL-1 受体敲除小鼠在暴露于 UVB 辐射后出现表皮囊肿并表现出改变的先天免疫反应》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Nikhil N Kulkarni , Christopher A Adase , Ling-Juan Zhang , Andrew W Borkowski , Fengwu Li , James A Sanford , Daniel J Coleman , Carlos Aguilera , Arup K Indra , Richard L Gallo 等完成。促进了肿瘤的精准治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤靶向药物及精准治疗临床研究内容关键词：

表皮囊肿,IL-1受体,促炎细胞因子,肿瘤坏死因子,巨噬细胞

肿瘤靶向治疗基因检测临床应用结果

在这项研究中，我们观察到缺乏 IL-1 受体 (IL-1R) (IL1r-/-) 或缺乏 IL1-β 的小鼠在长期暴露于 UVB 后会出现多个表皮囊肿。在 IL1r-/- 小鼠中发育的囊肿的特征是存在毛囊标志物 Sox 9、角蛋白 10 和 14，以及正常的黑素细胞分布和类视黄醇 X 受体-α 表达。 IL1r-/- 小鼠中囊肿发生率的增加与较少的皮肤炎症相关，其特征是巨噬细胞的募集减少，并且与野生型小鼠相比，它们的皮肤也保持了表皮屏障功能。暴露于 UVB 后 IL1r-/- 小鼠皮肤的转录分析显示促炎细胞因子如肿瘤坏死因子-α 和 IL-6 的基因表达降低。在体外，与野生型细胞相比，源自 IL1r-/- 小鼠的原代角质形成细胞对 UVB 引发的细胞死亡具有更强的抵抗力，并且在没有 IL-1R 的情况下，肿瘤坏死因子-α 的释放被完全阻断。这些观察结果说明了一种与小鼠缺乏 IL-1R 信号传导相关的意想不到但突出的表型，并支持进一步研究 IL-1 配体在破坏 UVB 暴露后在表皮修复和先天免疫反应中的作用。

肿瘤发生与复发转移国际数据库描述：

In this study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r-/-) or deficient in IL1-β developed multiple epidermal cysts after chronic UVB exposure. Cysts that developed in IL1r-/- mice were characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution and retinoid X receptor-α expression. The increased incidence of cysts in IL1r-/- mice was associated with less skin inflammation as characterized by decreased recruitment of macrophages, and their skin also maintained epidermal barrier function compared with wild-type mice. Transcriptional analysis of the skin of IL1r-/- mice after UVB exposure showed decreased gene expression of proinflammatory cytokines such as tumor necrosis factor-α and IL-6. In vitro, primary keratinocytes derived from IL1r-/- mice were more resistant to UVB-triggered cell death compared with wild-type cells, and tumor necrosis factor-α release was completely blocked in the absence of IL-1R. These observations illustrate an unexpected yet prominent phenotype associated with the lack of IL-1R signaling in mice and support further investigation into the role of IL-1 ligands in epidermal repair and innate immune response after damaging UVB exposure.