STAT/SOCS在银屑病发病机制中的作用

被引：3

作者：

陈飚

孙乐栋

张堂德

机构：

[1] 南方医科大学珠江医院皮肤科

来源：

皮肤性病诊疗学杂志 | 2013年 / 20卷 / 05期

关键词：

银屑病; STAT; SOCS;

D O I：

暂无

中图分类号：

R758.63 [牛皮癣（银屑病）];

学科分类号：

100206 ;

摘要：

银屑病的发病可能与异常活化的Th1细胞分泌IFN-γ等细胞因子有关,这些细胞因子主要通过Jak/STAT信号传导通路实现胞内信息传递,诱导一系列炎症相关基因的过度表达,促使银屑病发生发展。STAT1、STAT3、SOCS1、SOCS3在银屑病皮损角质形成细胞内的表达升高,STAT1、STAT3的异常活化可以促进细胞过度的分化增殖并抑制细胞凋亡,而SOCS1、SOCS3能抑制Jak/STAT信号传导通路的信息传递。银屑病角质形成细胞内STAT1、STAT3和SOCS1、SOCS3的表达水平可能是治疗银屑病的潜在药物作用靶点。

引用

页码：359 / 361

页数：3

共 22 条

[1] Altered keratin 17 peptide ligands inhibit in vitro proliferation of keratinocytes and T cells isolated from patients with psoriasis [J].

Shen, Zhu ;

Chen, Ling ;

Liu, Yu-F ;

Gao, Tian-W. ;

Wang, Gang ;

Fan, Xue-L. ;

Fan, Jian-Y. ;

Fan, Ping-S. ;

Li, Chun-Y. ;

Liu, Bin ;

Dang, Yu-P. ;

Li, Cheng-X. .

JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 2006, 54 (06) :992-1002

[2] Inflammatory cytokines in vascular dysfunction and vascular disease [J].

Sprague, Alexander H. ;

Khalil, Raouf A. .

BIOCHEMICAL PHARMACOLOGY, 2009, 78 (06) :539-552

[3]

The STATs of cancer — new molecular targets come of age. Hua Yu,Richard Jove. Nature Reviews Cancer . 2004

[4]

STAT 3 links activated keratinocytes andimm unocytes requ ired for deve lopm en t ofpsorias is in a nove l transgen ic m ouse m ode l. SANO S,CHAN K S,CARBA JAL S,et a l. N atM ed . 2005

[5]

SOCS1: a potent and multifaceted regulator of cytokines and cell‐mediated inflammation[J] . G. M.Davey,W. R.Heath,R.Starr. &nbspTissue Antigens . 2005 (1)

[6] SOCS regulation of the JAK/STAT signalling pathway [J].

Croker, Ben A. ;

Kiu, Hiu ;

Nicholson, Sandra E. .

SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 2008, 19 (04) :414-422

[7]

Constitutive Activation of JAK3/STAT3 in Colon Carcinoma Tumors and Cell Lines[J] . Quan Lin,Raymond Lai,Lucian R. Chirieac,Changping Li,Vilmos A. Thomazy,Ioannis Grammatikakis,George Z. Rassidakis,Wei Zhang,Yasushi Fujio,Keita Kunisada,Stanley R. Hamilton,Hesham M. Amin. &nbspThe American Journal of Pathology . 2005 (4)

[8] SOCS-3 inhibits IL-12-induced STAT4 activation by binding through its SH2 domain to the STAT4 docking site in the IL-12 receptor β2 subunit [J].

Yamamoto, K ;

Yamaguchi, M ;

Miyasaka, N ;

Miura, O .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 310 (04) :1188-1193

[9]

Jun signalling in the epidermis: From developmental defects to psoriasis and skin tumors[J] . Rainer Zenz,Erwin F. Wagner. &nbspInternational Journal of Biochemistry and Cell Biology . 2006 (7)

[10]

Inhibition of STAT3 signaling induces apoptosis and decreases survivin expression in primary effusion lymphoma. Aoki Y,Feldman G M,Tosato G. Blood . 2003

← 1 2 3 →