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Pathophysiology of moderate to severe plaque psoriasis: anti-IL-17 towards disease modification

机译:中度至重度斑块牛皮癣的病理生理学:抗IL-17疾病修饰

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摘要

Psoriasis is a chronic inflammatory disease that can be triggered by injury, trauma, infection and medications. Genetic and immunologic studies have highlighted the importance of the interleukin (10-23/T-helper 17 (Th17) pathway in systemic psoriasis pathogenesis. Main IL-23 is an upstream regulatory cytokine with direct effects on epidermal keratinocytes and other resident skin cells while L-17, a downstream molecule, can activate inflammatory responses in different cells across a diversity of organs. Disease modification could be achieved with drugs that can slow down the biological processes that cause the persistent inflammation in moderate to severe psoriasis. Early intervention with anti-IL-17 and anti-IL-23 agents in new-onset moderate to severe plaque psoriasis might modify the natural course of the disease. Perhaps we are not simply seeing a pharmacologic and mechanistic effect of new-generation biologics but eventually a disease modification process. In this short report we underline the main available data which supports an important role for IL-17 blockade and address whether these new drugs targeting the IL-23/IL-17 axis could be disease-modifying agents in plaque psoriasis. This type of data gains more relevance in the current pandemic era, where chronic patients undergoing earlier treatment may have better outcomes and consequently avoid constant hospital visits.
机译:银屑病是一种慢性炎症性疾病,可由损伤、创伤、感染和药物引起。遗传学和免疫学研究强调了白细胞介素(10-23/T-helper)17(Th17)通路在系统性银屑病发病机制中的重要性。主要的IL-23是一种上游调节性细胞因子,直接作用于表皮角质形成细胞和其他常驻皮肤细胞,而L-17是一种下游分子,可激活多种器官不同细胞的炎症反应。通过药物可以减缓导致中重度银屑病持续炎症的生物过程,从而实现疾病治疗。对新发中重度斑块型银屑病早期使用抗IL-17和抗IL-23药物干预可能会改变疾病的自然病程。也许我们看到的不仅仅是新一代生物制剂的药理学和机械效应,而是一个最终改变疾病的过程。在这篇简短的报告中,我们强调了支持IL-17阻断作用的主要可用数据,并讨论了这些针对IL-23/IL-17轴的新药是否可能是斑块型银屑病的疾病修饰剂。这类数据在当前大流行时代更具相关性,在这个时代,接受早期治疗的慢性病患者可能会有更好的结果,从而避免经常去医院就诊。

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