首页> 外文期刊>Arthritis and Rheumatism >STA-21, a Promising STAT-3 Inhibitor-That Reciprocally Regulates Thl7 and Treg Cells, Inhibits Osteoclastogenesis in Mice and Humans and Alleviates Autoimmune Inflammation in an Experimental Model of Rheumatoid Arthritis
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STA-21, a Promising STAT-3 Inhibitor-That Reciprocally Regulates Thl7 and Treg Cells, Inhibits Osteoclastogenesis in Mice and Humans and Alleviates Autoimmune Inflammation in an Experimental Model of Rheumatoid Arthritis

机译:STA-21,一种有前途的STAT-3抑制剂,可相互调节Th17和Treg细胞,抑制类风湿关节炎小鼠和人类的破骨细胞生成并减轻自身免疫性炎症。

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摘要

Rheumatoid arthritis (RA) is a multisystem autoimmune disease of unknown etiology that is characterized by a hyperplastic synovial membrane, also called pannus, capable of destroying adjacent articular cartilage and bone (1,2). Among the various pathologic events occurring in the affected joints, bone destruction is of utmost importance clinically because it is related to functional impairment and the progression of joint damage among patients with RA whose disease is in prolonged remission (3). Osteoclasts, which are specialized bone-resorbing cells regulated by RANKL and macrophage colony-stimulating factor (M-CSF), are mainly implicated in the development of bony erosion in RA(4,5).
机译:类风湿关节炎(RA)是一种病因不明的多系统自身免疫性疾病,其特征是增生性滑膜,也称为血管膜,能够破坏相邻的关节软骨和骨骼(1,2)。在受影响的关节中发生的各种病理事件中,骨破坏在临床上是最重要的,因为它与功能减退和疾病长期缓解的RA患者的关节损伤的进展有关(3)。破骨细胞是受RANKL和巨噬细胞集落刺激因子(M-CSF)调节的专门的骨吸收细胞,主要与RA骨质侵蚀的发生有关(4,5)。

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