Pathophysiology of psoriasis: Recent advances on IL-23 and TH17 cytokines

被引：320

作者：

Fitch E. ^{[1
]}

Harper E. ^{[1
]}

Skorcheva I. ^{[1
]}

Kurtz S.E. ^{[1
]}

Blauvelt A. ^{[1
]}

机构：

[1] Dermatology Service, Veterans Affairs Medical Center, Mail Code R and D 55, Portland, OR 97239

来源：

Current Rheumatology Reports | 2007年 / 9卷 / 6期

关键词：

Psoriasis; Th17 Cell; Psoriasis Lesion; Nonlesional Skin; Enic Mouse;

D O I：

10.1007/s11926-007-0075-1

中图分类号：

学科分类号：

摘要：

T helper (Th) 17 cells, a novel T-cell subset, have been implicated in the pathogenesis of psoriasis and other autoimmune inflammatory diseases. Interleukin (IL)-23 stimulates survival and proliferation of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. In psoriasis, IL-23 is overproduced by dendritic cells and keratinocytes, and this cytokine stimulates Th17 cells within dermis to make IL-17A and 1L-22. IL-22, in particular, drives keratinocyte hyperproliferation in psoriasis. Future targeting of these key cytokines is likely to lead to dramatic clinical improvement in patients with psoriasis. This review focuses on the numerous recent studies on the roles of IL-23 and Th17 cells in the pathogenesis of psoriasis. Copyright © 2007 by Current Medicine Group LLC.

引用

页码：461 / 467

页数：6

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