Center of Experimental Rheumatology, University Hospital Zürich, Switzerland.
Autoimmun Rev. 2011 Jul;10(9):519-24. doi: 10.1016/j.autrev.2011.04.001. Epub 2011 Apr 9.
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.
类风湿关节炎（RA）是一种慢性炎症性疾病，可导致关节破坏。滑膜成纤维细胞被认为是 RA 发病机制中的关键细胞，因为它们吸引和激活免疫细胞并产生基质降解酶。值得注意的是，来自 RA 患者的滑膜成纤维细胞被稳定激活，并在没有免疫细胞进一步刺激的情况下产生高水平的促病分子。越来越多的证据表明，基质细胞群体中的表观遗传变化可能在 RA 和其他慢性炎症性疾病的发病机制中起关键作用。在本综述中，我们讨论了表观遗传变化如何导致 RA 中滑膜成纤维细胞的稳定激活，以及表观基因组的变化如何改变免疫功能和炎症反应，从而促进慢性疾病的发展。
