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类风湿关节炎的病理机制

[Pathological mechanisms in rheumatoid arthritis].

作者信息

Tanaka Yoshiya

机构信息

First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.

出版信息

Nihon Rinsho. 2013 Jul;71(7):1147-52.

Abstract

Rheumatoid arthritis(RA) is a representative autoimmune disease characterized by systemic, chronic, destructive inflammatory synovitis and multiple organ manifestations, resulting in severe disability and mortality rates. Immune cells such as T cells, B cells, dendritic cells and macrophages and cellular interaction among them through cytokines and cell surface molecules plays a pivotal role in the pathological processes of RA. The accumulation of inflammatory cells, the self-perpetuation of inflammation and induction and/or activation of osteoclasts lead to cartilage and bone destruction and multiple organ manifestations. The importance of immune systems in the pathogenesis of RA has become apparent based on the clinical efficacy of biologic agents TNF, IL-6, CD28 and CD20. The research translation between bench and bedside would bring enormous progress in the treatment of RA.

摘要

类风湿关节炎(RA)是一种典型的自身免疫性疾病,其特征为全身性、慢性、破坏性炎症性滑膜炎及多器官表现,可导致严重残疾和死亡率。T细胞、B细胞、树突状细胞和巨噬细胞等免疫细胞以及它们之间通过细胞因子和细胞表面分子进行的细胞间相互作用在RA的病理过程中起关键作用。炎症细胞的积聚、炎症的自我持续以及破骨细胞的诱导和/或激活导致软骨和骨破坏以及多器官表现。基于生物制剂TNF、IL-6、CD28和CD20的临床疗效,免疫系统在RA发病机制中的重要性已变得显而易见。基础研究与临床应用之间的转化研究将为RA的治疗带来巨大进展。

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