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首页> 外文期刊>Experimental dermatology >Langerhans cell markers CD1a and CD207 are the most rapidly responding genes in lesional psoriatic skin following adalimumab treatment
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Langerhans cell markers CD1a and CD207 are the most rapidly responding genes in lesional psoriatic skin following adalimumab treatment

机译：Langerhans细胞标志物CD1a和CD207是患有Adalimalab治疗后损伤银屑病皮肤中最迅速的响应基因

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TNF alpha-, IL-23-and IL-17-targeting drugs are highly effective in the treatment of psoriasis. However, the precise molecular mechanism remains unknown. In psoriatic skin, the presence of Langerhans cells (LCs) is reduced, but the role of LC is poorly understood. The purpose of this study was to investigate the impact of TNF alpha and IL-23/IL-17 on the presence of LC in the skin during treatment. Therefore, psoriatic skin was investigated before and after 4 days of adalimumab or ustekinumab treatment. Furthermore, TNF alpha and IL-17A stimulation was investigated in an ex vivo model of epidermis and dermis from healthy normal skin kept in cultures at an air-liquid interphase for 4 days. In a gene array analysis, we found that the two LC markers, CD1a and CD207, were among the most up-or downregulated genes in psoriatic skin after anti-TNF alpha therapy. Validation showed that both mRNA expression and protein level followed the same pattern and became significantly upregulated after 4 days of treatment. No changes were seen after ustekinumab treatment. In the ex vivo skin model, a decrease in the CD1a level was seen after TNF alpha stimulation and it was caused by LC migration from epidermis. No response in LC migration was seen after IL-17A stimulation. Taken together, we demonstrated that changes in the LC level in epidermis precede the histological and clinical changes during adalimumab treatment in psoriatic skin. Furthermore, TNF alpha plays a prominent role in orchestrating LC migration in the skin. This seems not to be the true for the IL-23/IL-17A pathway.
机译：TNFα，IL-23和IL-17靶向药物在治疗牛皮癣方面具有高度有效。然而，精确的分子机制仍然未知。在银屑病皮肤中，朗格汉斯细胞（LCS）的存在降低，但LC的作用理解得很差。本研究的目的是研究TNFα和IL-23 / IL-17在治疗期间皮肤中LC的存在的影响。因此，在Adalimalab或Ustekinumab治疗的4天之前和之后研究了银屑病皮肤。此外，在表皮的前体内模型中研究了TNFα和IL-17A刺激，从健康正常皮肤处保存在空气 - 液体间的健康正常皮肤中4天。在基因阵列分析中，我们发现两种LC标记，CD1A和CD207是抗TNFα治疗后银屑病皮肤中最升高或下调的基因。验证表明，MRNA表达和蛋白质水平均匀呈现相同的模式，并且在治疗4天后显着上调。在Ustekinumab治疗后没有看到任何变化。在离体皮肤模型中，在TNFα刺激后看到CD1a水平的降低，并且由表皮的LC迁移引起。在IL-17A刺激后看到LC迁移中没有回应。我们占据了，我们证明了表皮的LC水平的变化在人物性皮肤中的Adalimalab治疗过程中的组织学和临床变化之前。此外，TNF alpha在策划皮肤中的LC迁移方面发挥着突出的作用。对于IL-23 / IL-17A途径而言，这似乎不是真的。

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