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特应性皮炎中的细胞因子和表皮脂质异常:系统评价。

Cytokines and Epidermal Lipid Abnormalities in Atopic Dermatitis: A Systematic Review.

机构信息

Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA.

出版信息

Cells. 2023 Dec 8;12(24):2793. doi: 10.3390/cells12242793.

Abstract

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease and presents a major public health problem worldwide. It is characterized by a recurrent and/or chronic course of inflammatory skin lesions with intense pruritus. Its pathophysiologic features include barrier dysfunction, aberrant immune cell infiltration, and alterations in the microbiome that are associated with genetic and environmental factors. There is a complex crosstalk between these components, which is primarily mediated by cytokines. Epidermal barrier dysfunction is the hallmark of AD and is caused by the disruption of proteins and lipids responsible for establishing the skin barrier. To better define the role of cytokines in stratum corneum lipid abnormalities related to AD, we conducted a systematic review of biomedical literature in PubMed from its inception to 5 September 2023. Consistent with the dominant T2 skewness seen in AD, type 2 cytokines were featured prominently as possessing a central role in epidermal lipid alterations in AD skin. The cytokines associated with T1 and T17 were also identified to affect barrier lipids. Considering the broad cytokine dysregulation observed in AD pathophysiology, understanding the role of each of these in lipid abnormalities and barrier dysfunction will help in developing therapeutics to best achieve barrier homeostasis in AD patients.

摘要

特应性皮炎(AD)是最常见的慢性炎症性皮肤病,也是全球范围内的一个主要公共卫生问题。其特征为反复发作和/或慢性炎症性皮肤损伤,伴有剧烈瘙痒。其病理生理特征包括屏障功能障碍、异常免疫细胞浸润以及与遗传和环境因素相关的微生物组改变。这些成分之间存在复杂的相互作用,主要由细胞因子介导。表皮屏障功能障碍是 AD 的标志,是由负责建立皮肤屏障的蛋白质和脂质的破坏引起的。为了更好地定义细胞因子在与 AD 相关的角质层脂质异常中的作用,我们对 PubMed 从建立到 2023 年 9 月 5 日的生物医学文献进行了系统综述。与 AD 中观察到的主导 T2 偏斜一致,2 型细胞因子作为 AD 皮肤表皮脂质改变的核心作用而突出。与 T1 和 T17 相关的细胞因子也被确定会影响屏障脂质。考虑到 AD 病理生理学中广泛存在的细胞因子失调,了解这些细胞因子在脂质异常和屏障功能障碍中的作用将有助于开发治疗方法,以最好地实现 AD 患者的屏障稳态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6364/10741881/7a44ca80cd43/cells-12-02793-g001.jpg

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