Signal transduction and Th17 cell differentiation

被引:60
|
作者
O'Shea, John J. [1 ]
Steward-Tharp, Scott M. [1 ,2 ]
Laurence, Arian [1 ]
Watford, Wendy T. [1 ]
Wei, Lai [1 ]
Adamson, Adewole S. [1 ,3 ]
Fan, Samuel [1 ,4 ]
机构
[1] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA
[2] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20814 USA
[3] Harvard Mit Div Hlth Sci & Technol, Boston, MA 02115 USA
[4] Bradley Univ, Dept Biol, Peoria, IL 61625 USA
关键词
Th17; IL-17; Signal transduction; Transcription factor; Lymphocyte differentiation; Cytokines; Chromatin; ARYL-HYDROCARBON RECEPTOR; ROR-GAMMA-T; INTERFERON-REGULATORY FACTOR-4; GROWTH-FACTOR-BETA; COLLAGEN-INDUCED ARTHRITIS; HELPER TYPE-1 CELLS; HYPER-IGE SYNDROME; TGF-BETA; RETINOIC-ACID; CUTTING EDGE;
D O I
10.1016/j.micinf.2009.04.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The paradigm of effector T helper cell differentiation into either Th1 or Th2 lineages has been notably shaken by the discovery of a third lineage of cells that selectively produce interleukin (IL)-17. Characterization of this new subset, referred to as Th17, has provided exciting new insights into immunoregulation, host defense and the pathogenesis of autoimmune diseases. Additionally, the discovery of this T cell subset has offered a fresh look at such concepts as lineage commitment and terminal differentiation. The transcriptional regulatory events and epigenetic modifications that control these processes are diverse and complex, and despite the rapid pace at which data continue to accumulate, many questions remain to be answered. Here we review our current understanding of the signaling pathways, molecular interactions and transcriptional events that lead to Th17 differentiation and effector function, as well as the epigenetic modifications that accompany them. Published by Elsevier Masson SAS.
引用
收藏
页码:599 / 611
页数:13
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