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首页> 外文期刊>Journal of dermatological science >Erratum to 'Neutrophil-dominant psoriasis-like skin inflammation induced by epidermal-specific expression of Raf in mice' (J. Dermatol. Sci. 58 (2010) 28-35)
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Erratum to 'Neutrophil-dominant psoriasis-like skin inflammation induced by epidermal-specific expression of Raf in mice' (J. Dermatol. Sci. 58 (2010) 28-35)

机译：对“由Raf的表皮特异性表达诱导的嗜中性粒细胞样牛皮癣样皮肤炎症的勘误”（J. Dermatol。Sci。58（2010）28-35）

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BACKGROUND: Raf is one of the downstream effectors of Ras GTPases. The induction of Raf in the epidermis causes the proliferation of keratinocytes and epidermal hyperplasia. However, skin inflammation accompanying Ras-induced epidermal reactions has not been fully delineated. OBJECTIVE: The aim of this study was to characterize inflammatory reactions induced by epidermal-specific Raf expression and to elucidate its role in skin inflammation. METHODS: K14-Raf:ER transgenic mice, in which the 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor (ER) ligand binding domain-Raf fusion gene was expressed under control of the keratin 14 promoter, were used to characterize inflammatory reactions induced by Raf expression in the epidermis. RESULTS: A single topical application of 4OHT induced the expression of phosphorylated extracellular signal-related kinase 1/2 and elicited neutrophil-dominant inflammatory infiltrates in the skin. The Raf expression also rapidly induced the production of several cytokines and chemokines, including VEGF and CXCL1, by keratinocytes and inmouse skin in vivo. Furthermore, CD4-positive cells from regional lymph nodes had the potential to differentiate into IFNg- and IL17-producing cells. Treatment with an anti-Gr-1 antibody diminished the Raf-induced cutaneous inflammation and partially reversed the epidermal hyperplasia and hyperkeratosis. CONCLUSION: Activation of the Raf signaling pathway is involved in the epidermal hyperplasia and the neutrophil-dominant cutaneous inflammatory reactions which are characteristics of psoriasis.
机译：背景：Raf是Ras GTPases的下游效应子之一。表皮中Raf的诱导引起角质形成细胞的增殖和表皮增生。然而，还没有完全描述伴随Ras诱导的表皮反应的皮肤炎症。目的：本研究的目的是表征表皮特异性Raf表达诱导的炎症反应，并阐明其在皮肤炎症中的作用。方法：使用K14-Raf：ER转基因小鼠，在角蛋白14启动子的控制下表达4-羟基他莫昔芬（4OHT）反应性突变雌激素受体（ER）配体结合域-Raf融合基因，以表征炎症反应由表皮中的Raf表达诱导。结果：4OHT的局部应用诱导磷酸化的细胞外信号相关激酶1/2的表达，并引起皮肤中性粒细胞占主导的炎症浸润。 Raf表达还迅速诱导角化细胞和体内小鼠皮肤产生几种细胞因子和趋化因子，包括VEGF和CXCL1。此外，来自区域淋巴结的CD4阳性细胞有可能分化为产生IFNg和IL17的细胞。用抗Gr-1抗体治疗可减少Raf引起的皮肤炎症，并部分逆转表皮增生和角化过度。结论：Raf信号通路的激活与牛皮癣的特征是表皮增生和以中性粒细胞为主的皮肤炎症反应有关。

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