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本文引用的文献

1
Cathelicidin antimicrobial peptide LL-37 in psoriasis enables keratinocyte reactivity against TLR9 ligands.银屑病中的抗菌肽 LL-37 使角质形成细胞对 TLR9 配体产生反应性。
J Invest Dermatol. 2012 Jan;132(1):135-43. doi: 10.1038/jid.2011.259. Epub 2011 Aug 18.
2
Cytosolic DNA triggers inflammasome activation in keratinocytes in psoriatic lesions.细胞质 DNA 触发银屑病皮损中角质形成细胞中的炎性体激活。
Sci Transl Med. 2011 May 11;3(82):82ra38. doi: 10.1126/scitranslmed.3002001.
3
Human slan (6-sulfo LacNAc) dendritic cells are inflammatory dermal dendritic cells in psoriasis and drive strong TH17/TH1 T-cell responses.人唾液酸(6-硫酸乳糖胺)树突状细胞是银屑病中的炎症性真皮树突状细胞,可驱动强烈的 TH17/TH1 T 细胞应答。
J Allergy Clin Immunol. 2011 Mar;127(3):787-94.e1-9. doi: 10.1016/j.jaci.2010.12.009.
4
Expression of antimicrobial peptides and proteins in etanercept-treated psoriasis patients.依那西普治疗的银屑病患者中抗菌肽和蛋白质的表达
Regul Pept. 2011 Apr 11;167(2-3):163-6. doi: 10.1016/j.regpep.2011.02.001. Epub 2011 Feb 12.
5
Increased serum leucine, leucine-37 levels in psoriasis: positive and negative feedback loops of leucine, leucine-37 and pro- or anti-inflammatory cytokines.银屑病患者血清亮氨酸、亮氨酸-37 水平升高:亮氨酸、亮氨酸-37 和促炎/抗炎细胞因子的正、负反馈环。
Hum Immunol. 2010 Dec;71(12):1161-71. doi: 10.1016/j.humimm.2010.09.005. Epub 2010 Sep 16.
6
The human cathelicidin hCAP18/LL-37: a multifunctional peptide involved in mycobacterial infections.人源抗菌肽 hCAP18/LL-37:参与分枝杆菌感染的多功能肽。
Peptides. 2010 Sep;31(9):1791-8. doi: 10.1016/j.peptides.2010.06.016. Epub 2010 Jun 25.
7
Narrowband ultraviolet B treatment improves vitamin D balance and alters antimicrobial peptide expression in skin lesions of psoriasis and atopic dermatitis.窄谱中波紫外线治疗可改善银屑病和特应性皮炎皮损中的维生素 D 平衡,并改变抗菌肽的表达。
Br J Dermatol. 2010 Aug;163(2):321-8. doi: 10.1111/j.1365-2133.2010.09767.x. Epub 2010 Mar 17.
8
Control of cutaneous antimicrobial peptides by vitamin D3.维生素 D3 对皮肤抗菌肽的调控作用。
Arch Dermatol Res. 2010 Aug;302(6):401-8. doi: 10.1007/s00403-010-1045-4. Epub 2010 Mar 10.
9
Vitamin D and innate immunity.维生素 D 与先天免疫。
Dermatol Ther. 2010 Jan-Feb;23(1):13-22. doi: 10.1111/j.1529-8019.2009.01287.x.
10
Self-RNA-antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8.自身RNA-抗菌肽复合物通过TLR7和TLR8激活人树突状细胞。
J Exp Med. 2009 Aug 31;206(9):1983-94. doi: 10.1084/jem.20090480. Epub 2009 Aug 24.

抗菌肽在银屑病发病机制中的作用。

Antimicrobial peptides in the pathogenesis of psoriasis.

机构信息

Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

出版信息

J Dermatol. 2012 Mar;39(3):225-30. doi: 10.1111/j.1346-8138.2011.01483.x.

DOI:10.1111/j.1346-8138.2011.01483.x
PMID:22352846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3527011/
Abstract

One characteristic abnormality of lesional skin in psoriasis is the excessive production of antimicrobial peptides and proteins (AMPs). AMPs typically are small (12-50 amino acids), have positive charge and amphipathic structure, and are found in all living organisms including mammals, insects, plants and invertebrates. These peptides are best known for their integral role in killing pathogenic microorganisms; however, in vertebrates, they are also capable of modifying host inflammatory responses by a variety of mechanisms. In psoriatic lesions, many AMPs are highly expressed, and especially the associations between psoriasis and cathelicidin, β-defensins or S100 proteins have been well studied. Among them, a cathelicidin peptide, LL-37, has been highlighted as a modulator of psoriasis development in recent years. AMPs had been thought to worsen psoriatic lesions but recent evidence has also suggested the possibility that the induction of AMPs expression might improve aspects of the disease. Further investigations are needed to uncover a previously underappreciated role for AMPs in modulating the immune response in psoriasis, and to improve disease without the risks of systemic immunosuppressive approaches.

摘要

银屑病皮损的一个特征性异常是抗菌肽和蛋白质(AMPs)的过度产生。AMPs 通常很小(12-50 个氨基酸),带正电荷和两亲性结构,存在于包括哺乳动物、昆虫、植物和无脊椎动物在内的所有生物中。这些肽以其在杀死致病微生物方面的重要作用而闻名;然而,在脊椎动物中,它们还通过多种机制能够调节宿主炎症反应。在银屑病皮损中,许多 AMPs 表达水平升高,尤其是银屑病与抗菌肽、β-防御素或 S100 蛋白之间的关联已得到深入研究。其中,一种抗菌肽 LL-37 近年来被强调为银屑病发展的调节剂。AMPs 曾被认为会加重银屑病皮损,但最近的证据也表明,诱导 AMPs 表达可能改善疾病的某些方面。需要进一步研究以揭示 AMPs 在调节银屑病免疫反应方面以前被低估的作用,并改善疾病而不带来全身免疫抑制方法的风险。