Angelotti Francesca, Parma Alice, Cafaro Giacomo, Capecchi Riccardo, Alunno Alessia, Puxeddu Ilaria
Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
Rheumatology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
Clin Exp Rheumatol. 2017 May-Jun;35(3):368-378. Epub 2017 Jun 7.
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease influenced by both genetic and environmental factors. It has been postulated that a high-risk genetic background, in combination with epigenetic marks and environmental exposures, leads to a cascade of events inducing synovitis and consequent destructive arthritis. The clinical picture of joint involvement in RA is the result of chronic inflammation of the synovium, characterised by interactions of resident cells such as fibroblast-like synoviocytes (FLS) with cells of the innate (e.g. macrophages, dendritic cells, mast cells and NK cells, neutrophils) and adaptive immune system (e.g. B and T lymphocytes). Currently, our understanding of the role of innate and adaptive immunity in the pathogenesis of RA is expanding. The concept of how immune responses contribute to the disease has dramatically evolved over the last 50 years. Shedding some light on the different aspects of RA pathogenesis will help to identify new targets for the development of disease-modifying therapies. Thus, in this review we report new insights in RA pathogenesis, resulting from a literature research date published in the last year.
类风湿关节炎（RA）是一种受遗传和环境因素影响的慢性炎症性自身免疫性疾病。据推测，高风险遗传背景与表观遗传标记和环境暴露相结合，会引发一系列事件，导致滑膜炎及随后的破坏性关节炎。RA关节受累的临床表现是滑膜慢性炎症的结果，其特征是成纤维样滑膜细胞（FLS）等驻留细胞与固有免疫系统（如巨噬细胞、树突状细胞、肥大细胞、NK细胞、中性粒细胞）和适应性免疫系统（如B和T淋巴细胞）的细胞相互作用。目前，我们对固有免疫和适应性免疫在RA发病机制中的作用的理解正在不断扩展。在过去50年里，免疫反应如何导致该疾病的概念发生了巨大演变。阐明RA发病机制的不同方面将有助于确定疾病改善疗法开发的新靶点。因此，在本综述中，我们报告了去年发表的文献研究得出的关于RA发病机制的新见解。
