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对外周血单核细胞进行的全基因组表达分析揭示了银屑病中的基因表达特征。

A global gene expression analysis of the peripheral blood mononuclear cells reveals the gene expression signature in psoriasis.

作者信息

Lee Sang-Keun, Jeon Eun-Kyoung, Kim Yu-Jin, Seo Sam-Hwa, Kim Chang-Deok, Lim Jong-Soon, Lee Jeung-Hoon

机构信息

College of Oriental Medicine, Daejeon University, Daejeon, Korea.

出版信息

Ann Dermatol. 2009 Aug;21(3):237-42. doi: 10.5021/ad.2009.21.3.237. Epub 2009 Aug 31.

Abstract

BACKGROUND

Psoriasis is a chronic inflammatory skin disease that affects approximately 1~3% of the general population.

OBJECTIVE

We performed cDNA microarray analysis with using the dendrimer labelling method to investigate the gene expression profile in the peripheral blood mononuclear cells (PBMCs) of psoriatic patients.

METHODS

The peripheral blood mononuclear cells of 5 patients with psoriasis and 8 control subjects were used in the gene expression analyses of psoriasis.

RESULTS

We identified 212 differentially expressed genes that showed at least a two-fold induction and/or reduction in psoriatic patients. Among those, 63 genes, including CD44, CD56 and IL7R, were induced, while 139 genes, including the sphingosine kinase 1 and p16-INK genes, were reduced in the psoriatic patients.

CONCLUSION

We can speculate that these genes may have a role for the pathogenesis of psoriasis via their affecting different cellular functions. Our results suggest a possible mechanism by which activated immune cells migrate from the blood to the skin in psoriatic patients, and we provide novel putative targets for developing drugs to treat psoriasis.

摘要

背景

银屑病是一种慢性炎症性皮肤病,影响着约1%至3%的普通人群。

目的

我们采用树枝状大分子标记法进行cDNA微阵列分析,以研究银屑病患者外周血单个核细胞(PBMC)中的基因表达谱。

方法

选取5例银屑病患者和8例对照受试者的外周血单个核细胞进行银屑病的基因表达分析。

结果

我们鉴定出212个差异表达基因,这些基因在银屑病患者中表现出至少两倍的诱导和/或下调。其中,包括CD44、CD56和IL7R在内的63个基因被诱导,而包括鞘氨醇激酶1和p16-INK基因在内的139个基因在银屑病患者中被下调。

结论

我们可以推测,这些基因可能通过影响不同的细胞功能在银屑病的发病机制中发挥作用。我们的结果提示了银屑病患者中活化免疫细胞从血液迁移至皮肤的一种可能机制,并且我们为开发治疗银屑病的药物提供了新的潜在靶点。

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Immunopathogenic mechanisms in psoriasis.银屑病的免疫致病机制。
Clin Exp Immunol. 2004 Jan;135(1):1-8. doi: 10.1111/j.1365-2249.2004.02310.x.
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