Interleukin-17-producing T helper cells in autoimmunity

被引:119
作者
Hemdan, Nasr Ya. [1 ,2 ]
Birkenmeier, Gerd [3 ]
Wichmann, Gunnar [1 ]
Abu El-Saad, Ahmed M. [2 ]
Krieger, Thorsten [4 ]
Conrad, Karsten [5 ]
Sack, Ulrich [6 ]
机构
[1] Univ Leipzig, ENT Res Lab, Dept Otolaryngol Head & Neck Surg, Fac Med, Leipzig, Germany
[2] Univ Alexandria, Fac Sci, Dept Zool, Alexandria, Egypt
[3] Univ Leipzig, Inst Biochem, Fac Med, Leipzig, Germany
[4] Asculab Hamburg, Hamburg, Germany
[5] Univ Dresden, Fac Med, Inst Immunol, Dresden, Germany
[6] Univ Leipzig, Fac Med, Inst Clin Immunol, Leipzig, Germany
关键词
Autoimmune diseases; Cytokines; IL-17; Interleukin; 17; Regulatory T cells; T helper 17 (T(H)17) cells; GROWTH-FACTOR-BETA; COLLAGEN-INDUCED ARTHRITIS; CHEMOKINE RECEPTOR CXCR3; ENTERICA SEROVAR ENTERITIDIS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; INFLAMMATORY-BOWEL-DISEASE; CENTRAL-NERVOUS-SYSTEM; TH17; CELLS; TGF-BETA; RHEUMATOID-ARTHRITIS;
D O I
10.1016/j.autrev.2010.07.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
With all the incredible progress in scientific research over the past two decades, the trigger of the majority of autoimmune disorders remains largely elusive. Research on the biology of T helper type 17 (T(H)17) cells over the last decade not only clarified previous observations of immune regulations and disease manifestations, but also provided considerable information on the signaling pathways mediating the effects of this lineage and its seemingly dual role in fighting the invading pathogens on one hand, and in frightening the host by inducing chronic inflammation and autoimmunity on the other hand. In this context, recent reports have implicated T(H)17 cells in mediating host defense as well as a growing list of autoimmune diseases in genetically-susceptible individuals. Herein, we summarize the current knowledge on T(H)17 in autoimmunity with emphasis on its differentiation factors and some mechanisms involved in initiating pathological events of autoimmunity. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:785 / 792
页数:8
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