Targeting Th17 Effector Cytokines for the Treatment of Autoimmune Diseases

被引：27

作者：

Yamagata, Tetsuya ^{[1
]}

Skepner, Jill ^{[1
]}

Yang, Jianfei ^{[1
]}

机构：

[1] GlaxoSmithKline, Tempero, Cambridge, MA 02139 USA

来源：

ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS | 2015年 / 63卷 / 06期

关键词：

Th17; IL-17; IL-22; IL-26; Autoimmune disease; ANTI-INTERLEUKIN-17; MONOCLONAL-ANTIBODY; COLLAGEN-INDUCED ARTHRITIS; T-CELL POPULATION; RHEUMATOID-ARTHRITIS; HOST-DEFENSE; INTERLEUKIN; 22; GENE-EXPRESSION; CUTTING EDGE; DOUBLE-BLIND; INTESTINAL INFLAMMATION;

D O I：

10.1007/s00005-015-0362-x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Interleukin (IL)-17-producing T cells, especially T helper (Th)17 cells, play a critical role in the pathogenesis of a variety of autoimmune inflammatory diseases. The pathogenic function of Th17 cells results from their production of Th17 effector cytokines, namely IL-17 (or IL-17A), IL-17F, IL-22 and IL-26. The importance of IL-17 has been demonstrated by antibody neutralization studies in both animal models of autoimmune diseases as well as in human clinical trials. This review highlights the current knowledge of the clinical aspects of the Th17 cytokines as well as therapeutic antibodies against IL-17, IL-17F, IL-17 receptor, IL-22, IL-26 and granulocyte macrophage colony-stimulating factor for the future treatment of autoimmune inflammatory diseases.

引用

页码：405 / 414

页数：10

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