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Cell Prolif. 2010 Jun;43(3):321-5. doi: 10.1111/j.1365-2184.2010.00672.x.
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The heterogeneity of the germinative compartment in human epidermis and its implications in pathogenesis.人类表皮生发层的异质性及其在发病机制中的意义。
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Smoking and risk of incident psoriasis among women and men in the United States: a combined analysis.美国人群中吸烟与银屑病发病风险:合并分析。
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本文引用的文献

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Origin of threshold behaviour in psoriatic skin.银屑病皮肤中阈值行为的起源。
Dermatology. 2008;217(4):295-8. doi: 10.1159/000151354. Epub 2008 Aug 15.
2
Apoptosis in psoriatic epidermis.银屑病表皮中的细胞凋亡。
J Cutan Pathol. 2008 Mar;35(3):346. doi: 10.1111/j.1600-0560.2007.00795.x.
3
Polymorphisms of the IL12B and IL23R genes are associated with psoriasis.白细胞介素12B(IL12B)基因和白细胞介素23受体(IL23R)基因的多态性与银屑病相关。
J Invest Dermatol. 2008 Jul;128(7):1653-61. doi: 10.1038/sj.jid.5701255. Epub 2008 Jan 24.
4
Psoriasis is associated with increased beta-defensin genomic copy number.银屑病与β-防御素基因组拷贝数增加有关。
Nat Genet. 2008 Jan;40(1):23-5. doi: 10.1038/ng.2007.48. Epub 2007 Dec 2.
5
Redistribution of LRIG proteins in psoriasis.LRIG蛋白在银屑病中的重新分布。
J Invest Dermatol. 2008 May;128(5):1192-5. doi: 10.1038/sj.jid.5701175. Epub 2007 Nov 22.
6
Epidermal homeostasis: do committed progenitors work while stem cells sleep?表皮稳态:定向祖细胞在干细胞休眠时发挥作用吗?
Nat Rev Mol Cell Biol. 2008 Jan;9(1):82-8. doi: 10.1038/nrm2292.
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Kinetics of cell division in epidermal maintenance.表皮维持中细胞分裂的动力学
Phys Rev E Stat Nonlin Soft Matter Phys. 2007 Aug;76(2 Pt 1):021910. doi: 10.1103/PhysRevE.76.021910. Epub 2007 Aug 9.
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Pathogenesis and clinical features of psoriasis.银屑病的发病机制与临床特征
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9
The evolution of the psoriatic lesion.银屑病皮损的演变。
Br J Dermatol. 2007 Jul;157(1):4-15. doi: 10.1111/j.1365-2133.2007.07907.x.
10
A single type of progenitor cell maintains normal epidermis.单一类型的祖细胞维持正常表皮。
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表皮动力学改变是产生银屑病表型所必需的:再评价。

Epidermal kinetic alterations required to generate the psoriatic phenotype: a reappraisal.

机构信息

Department of Dermatology, Hôpital Universitaire Erasme, Brussels, Belgium.

出版信息

Cell Prolif. 2010 Jun;43(3):321-5. doi: 10.1111/j.1365-2184.2010.00672.x.

DOI:10.1111/j.1365-2184.2010.00672.x
PMID:20546247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6496873/
Abstract

OBJECTIVES

Although there have been major advances in understanding immunopathogenesis of psoriasis, the basic processes causing psoriatic morphology remain to be identified.

MATERIALS AND METHODS

Our group has designed a systematic review of studies (1962-2009) on keratinocyte kinetics in psoriasis. We obtained data from MEDLINE, PubMed, Current Contents, reference lists and specialist textbooks. A general equation for evolution of the differentiated epidermis has been analysed. Necessary conditions for observed qualitative change in homeostasis between normal skin and established psoriatic lesions were determined.

RESULTS AND DISCUSSION

Increase in the number of cell divisions (or imbalance in symmetric division rates of committed progenitor cells) and/or decrease in physiological apoptosis in the germinative compartment, together with feedback loops that limit thickening of the skin, are required to generate psoriatic morphology, that is, to increase the absolute size but decrease relative size of the differentiated cell compartment with respect to the germinative compartment.

摘要

目的

尽管人们对银屑病的免疫发病机制已有了深入的了解,但导致银屑病形态学的基本过程仍有待确定。

材料和方法

我们小组对银屑病角朊细胞动力学的研究(1962-2009 年)进行了系统综述。我们从 MEDLINE、PubMed、Current Contents、参考文献列表和专业教科书获取数据。对分化表皮的进化进行了一般方程分析。确定了在正常皮肤和已建立的银屑病病变之间的体内平衡中观察到的定性变化的必要条件。

结果与讨论

增加细胞分裂的数量(或对称分裂率失衡的定向祖细胞)和/或减少有丝分裂中胚层的生理凋亡,与限制皮肤增厚的反馈回路一起,是产生银屑病形态学所必需的,即增加分化细胞区室相对于有丝分裂中胚层的绝对大小,但减小相对大小。