欢迎来到《四川大学学报(医学版)》
尹耕, 文富强. 类风湿关节炎的炎症免疫机制及疾病活动性的评估[J]. 四川大学学报(医学版), 2015, 46(2): 267-271.
引用本文: 尹耕, 文富强. 类风湿关节炎的炎症免疫机制及疾病活动性的评估[J]. 四川大学学报(医学版), 2015, 46(2): 267-271.
YIN Geng, WEN Fu-qiang. Immune Mediated Inflammatory Pathogenesis and Assessment of Disease Activity in Rheumatoid Arthritis[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 267-271.
Citation: YIN Geng, WEN Fu-qiang. Immune Mediated Inflammatory Pathogenesis and Assessment of Disease Activity in Rheumatoid Arthritis[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 267-271.

类风湿关节炎的炎症免疫机制及疾病活动性的评估

Immune Mediated Inflammatory Pathogenesis and Assessment of Disease Activity in Rheumatoid Arthritis

  • 摘要: 类风湿关节炎(rheumatoid arthritis,RA)是一种系统性慢性炎症性疾病,其基本病理特征是关节滑膜炎及血管翳形成。炎症是RA发生发展的基础和核心,但其炎症免疫机制尚不明确,本专题围绕RA的炎症及骨免疫代谢机制进行探讨,证实T细胞、B细胞、促炎因子网络及趋化因子均参与发病。此外,滑膜细胞、成骨细胞、破骨细胞等骨关节相关的结构细胞作为免疫调控下游的效应细胞,也广泛参与RA的炎症进展。RA的炎症与疾病活动性密切相关,对目前用于RA病情评估的多种方法进行比较,有利于规范应用及优化病情评估工具,从而制定治疗决策,改善患者预后。

     

    Abstract: Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease with synovitis and pannus formation as its basic pathologic features. Immune mediated inflammation is the core event in the occurrence and development of RA, but the inflammatory mechanism in RA pathogenesis remains unclear and needs more research to be illustrated. T cells, B cells, proinflammatory cytokine network and chemokines were confirmed to be involved in the process. In addition, the cells related to the structure of bone and joint, such as synovial cells, osteoblasts and osteoclasts, also participate in the inflammation progression of RA acting as the effector cells of immune regulation. The severity of inflammation of RA is closely related to disease activity. There are many kinds of tools for the assessment of disease activity of RA. The rationale use and optimization of these assessment tools will be helpful to make the treatment decision and improve the prognosis of RA.

     

© 2015 《四川大学学报(医学版)》编辑部 版权所有 cc

开放获取 本文遵循知识共享署名—非商业性使用4.0国际许可协议(CC BY-NC 4.0),允许第三方对本刊发表的论文自由共享(即在任何媒介以任何形式复制、发行原文)、演绎(即修改、转换或以原文为基础进行创作),必须给出适当的署名,提供指向本文许可协议的链接,同时标明是否对原文作了修改;不得将本文用于商业目的。CC BY-NC 4.0许可协议详情请访问 https://creativecommons.org/licenses/by-nc/4.0

/

返回文章
返回