Mechanisms of Disease: Interleukin-17 and Type 17 Helper T Cells.

被引：1106

作者：

Miossec, Pierre ^{[1
]}

Korn, Thomas ^{[2
]}

Kuchroo, Vijay K. ^{[3
]}

机构：

[1] Univ Lyon, Hop Edouard Herriot, Dept Immunol & Rheumatol, Clin Immunol Unit, F-69003 Lyon, France

[2] Tech Univ Munich, Dept Neurol, Munich, Germany

[3] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA

来源：

NEW ENGLAND JOURNAL OF MEDICINE | 2009年 / 361卷 / 09期

基金：

美国国家卫生研究院;

关键词：

GROWTH-FACTOR-BETA; ROR-GAMMA-T; CENTRAL-NERVOUS-SYSTEM; TGF-BETA; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; TH17; CELLS; AUTOIMMUNE INFLAMMATION; TRANSCRIPTION FACTOR; MULTIPLE-SCLEROSIS;

D O I：

10.1056/NEJMra0707449

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Type 17 helper T cells (Th17) - a third class of T cells - and their major cytokine, interleukin-17, are essential for the defense against certain fungi, extracellular bacteria, and Mycobacterium tuberculosis. Defective control of Th17 cells and production of interleukin-17 are prominent in chronic inflammation and several immunoinflammatory disorders. Monoclonal antibodies against cytokines produced by Th17 cells are being investigated in clinical trials. Copyright © 2009 Massachusetts Medical Society.

引用

页码：888 / 898

页数：11

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