JAK and STAT Signaling Molecules in Immunoregulation and Immune-Mediated Disease

被引：1195

作者：

O'Shea, John J. ^{[1
]}

Plenge, Robert ^{[2
,3
]}

机构：

[1] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA

[2] Brigham & Womens Hosp, Div Genet, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA

[3] Broad Inst & Harvard, Cambridge, MA 02142 USA

来源：

IMMUNITY | 2012年 / 36卷 / 04期

关键词：

GENOME-WIDE ASSOCIATION; REGULATORY T-CELLS; ACTIVE RHEUMATOID-ARTHRITIS; INHIBITOR TOFACITINIB CP-690,550; TRANSCRIPTION FACTOR; INADEQUATE RESPONSE; MITOCHONDRIAL STAT3; SUSCEPTIBILITY LOCI; GENE-EXPRESSION; SH2; DOMAIN;

D O I：

10.1016/j.immuni.2012.03.014

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The discovery of the Janus kinase (JAK)-signal transducer and activator of transcripton (STAT) signaling pathway, a landmark in cell biology, provided a simple mechanism for gene regulation that dramatically advanced our understanding of the action of hormones, interferons, colony-stimulating factors, and interleukins. As we learn more about the complexities of immune responses, new insights into the functions of this pathway continue to be revealed, aided by technology that permits genome-wide views. As we celebrate the 20th anniversary of the discovery of this paradigm in cell signaling, it is particularly edifying to see how this knowledge has rapidly been translated to human immune disease. Not only have genome-wide association studies demonstrated that this pathway is highly relevant to human autoimmunity, but targeting JAKs is now a reality in immune-mediated disease.

引用

页码：542 / 550

页数：9

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