Inflammatory memories: Is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis?

被引：53

作者：

Ospelt, Caroline ^{[1
,2
]}

Reedquist, Kris A. ^{[2
]}

Gay, Steffen ^{[1
]}

Tak, Paul P. ^{[2
]}

机构：

[1] Univ Zurich Hosp, Ctr Expt Rheumatol, CH-8091 Zurich, Switzerland

[2] Univ Amsterdam, Div Clin Immunol & Rheumatol, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands

来源：

AUTOIMMUNITY REVIEWS | 2011年 / 10卷 / 09期

关键词：

Epigenetics; Synovial fibroblasts; Rheumatoid arthritis; NF-KAPPA-B; TOLL-LIKE RECEPTORS; SYNOVIAL TISSUE; DEPENDENT TRANSCRIPTION; DNA HYPOMETHYLATION; EXPRESSION; ACETYLATION; METHYLATION; FIBROBLASTS; OSTEOARTHRITIS;

D O I：

10.1016/j.autrev.2011.04.001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Rheumatoid arthritis (RA) is a chronic inflammatory disease leading to joint destruction. Synovial fibroblasts are recognized as key cells in the pathogenesis of RA since they attract and activate immune cells and produce matrix degrading enzymes. Most notably synovial fibroblasts from patients with RA are stably activated and produce high levels of disease-promoting molecules without further stimulation by immune cells. Accumulating data suggest that epigenetic changes in stromal cell populations might be crucially involved in the pathology of RA and other chronic inflammatory diseases. In the current review, we discuss the mechanisms by which epigenetic changes might cause the stable activation of synovial fibroblasts in RA and how changes in the epigenome might alter immune function and inflammatory response and thereby promote the development of chronic diseases. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：519 / 524

页数：6

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