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本文引用的文献

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Effect of narrowband ultraviolet B therapy on serum vitamin D and cathelicidin (LL-37) in patients with chronic plaque psoriasis.窄谱中波紫外线治疗对慢性斑块状银屑病患者血清维生素 D 和抗菌肽(LL-37)的影响。
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β-Defensin 2 and 3 promote the uptake of self or CpG DNA, enhance IFN-α production by human plasmacytoid dendritic cells, and promote inflammation.β-防御素 2 和 3 促进自身或 CpG DNA 的摄取,增强人浆细胞样树突状细胞产生 IFN-α,并促进炎症反应。
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Human antimicrobial peptide LL-37 modulates proinflammatory responses induced by cytokine milieus and double-stranded RNA in human keratinocytes.人抗菌肽 LL-37 调节细胞因子环境和双链 RNA 在人角质形成细胞中诱导的促炎反应。
Biochem Biophys Res Commun. 2013 Apr 19;433(4):532-7. doi: 10.1016/j.bbrc.2013.03.024. Epub 2013 Mar 20.
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Psoriasin: a novel marker linked obesity with psoriasis.银屑病素:一个将肥胖与银屑病联系起来的新型标志物。
Dis Markers. 2013;34(1):33-9. doi: 10.3233/DMA-2012-120945.
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Cytosolic sensing of extracellular self-DNA transported into monocytes by the antimicrobial peptide LL37.胞质溶胶对单核细胞内抗菌肽 LL37 转运的细胞外自身 DNA 的感应。
Blood. 2012 Nov 1;120(18):3699-707. doi: 10.1182/blood-2012-01-401364. Epub 2012 Aug 27.
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Novel insights into the role of S100A8/A9 in skin biology.对 S100A8/A9 在皮肤生物学中作用的新认识。
Exp Dermatol. 2012 Nov;21(11):822-6. doi: 10.1111/j.1600-0625.2012.01571.x. Epub 2012 Aug 9.
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Psoriasis: rationale for targeting interleukin-17.银屑病:针对白细胞介素-17 的作用机制。
Br J Dermatol. 2012 Oct;167(4):717-24. doi: 10.1111/j.1365-2133.2012.11099.x.
8
S100A8 and S100A9 are messengers in the crosstalk between epidermis and dermis modulating a psoriatic milieu in human skin.S100A8 和 S100A9 是表皮和真皮相互交流的信息传递者,调节人类皮肤的银屑病微环境。
Biochem Biophys Res Commun. 2012 Jul 13;423(4):647-53. doi: 10.1016/j.bbrc.2012.05.162. Epub 2012 Jun 7.
9
Cathelicidin LL-37: a defense molecule with a potential role in psoriasis pathogenesis.抗菌肽 LL-37:一种在银屑病发病机制中具有潜在作用的防御分子。
Exp Dermatol. 2012 May;21(5):327-30. doi: 10.1111/j.1600-0625.2012.01459.x.
10
Vitamin D analog calcipotriol suppresses the Th17 cytokine-induced proinflammatory S100 "alarmins" psoriasin (S100A7) and koebnerisin (S100A15) in psoriasis.维生素 D 类似物卡泊三醇抑制 Th17 细胞因子诱导的银屑病促炎 S100“警报素”角蛋白 17(S100A7)和角蛋白 15(S100A15)。
J Invest Dermatol. 2012 May;132(5):1416-24. doi: 10.1038/jid.2011.486. Epub 2012 Mar 8.

对抗菌肽/警报素在银屑病免疫发病机制中的作用的新认识。

The new insight into the role of antimicrobial proteins-alarmins in the immunopathogenesis of psoriasis.

机构信息

Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, ul. Chalubinskiego 1, 50-368 Wroclaw, Poland.

Department of Dermatology and Allergology, Ludwig-Maximilian University, Thalkirchner Straße 48, 80539 Munich, Germany.

出版信息

J Immunol Res. 2014;2014:628289. doi: 10.1155/2014/628289. Epub 2014 May 8.

DOI:10.1155/2014/628289
PMID:24901012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4034501/
Abstract

The pathognesis of psoriasis still remains not fully elucidated. Recent advances favor the idea that interactions between innate and adaptive immune response drive inflammatory process in this disease. Innate antimicrobial peptides and proteins (AMPs) are diverse group of small molecules that provide the first line of defense against invading pathogens. In recent years, the novel functions of AMPs have been identified. There are three subclasses among AMPs that have gained the special interest as a potentially important player in the pathogenesis of psoriasis: cathelicidin, S100 proteins, and defensins. These AMPs have been shown to modulate and trigger host immune response in psoriasis acting as interplayer between innate and adaptive immune mechanisms. Overexpressed in psoriatic lesions, they prime immune cells for enhanced production of proinflammatory mediators and act as chemoattractant for leukocytes. Therefore, the novel term describing AMPs alarmins has been suggested. As multifunctional player in pathogenesis of psoriasis, AMPs may constitute potential target for therapeutic interventions. However, further investigations are required to establish the methods of downregulation of the aberrant proinflammatory functions of AMPs without increasing the risk of infections.

摘要

银屑病的发病机制仍不完全清楚。最近的研究进展支持这样一种观点,即先天免疫和适应性免疫反应之间的相互作用驱动了这种疾病的炎症过程。先天抗菌肽和蛋白质(AMPs)是小分子的多样化群体,为抵御入侵病原体提供了第一道防线。近年来,已经确定了 AMPs 的新功能。AMP 有三个亚类,它们作为银屑病发病机制中潜在的重要参与者而受到特别关注:抗菌肽、S100 蛋白和防御素。这些 AMP 已被证明在银屑病中调节和触发宿主免疫反应,作为先天和适应性免疫机制之间的介体。在银屑病皮损中过度表达,它们为免疫细胞增强产生促炎介质做好准备,并作为白细胞趋化因子。因此,提出了一个描述 AMPs 警报素的新术语。作为银屑病发病机制中的多功能参与者,AMPs 可能成为治疗干预的潜在靶点。然而,需要进一步的研究来确定下调 AMPs 异常促炎功能的方法,而不增加感染的风险。