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Cytokine-mediated signals as targets for treatment of rheumatoid arthritis: a JAK inhibitor in vitro and in vivo

机译:细胞因子介导的信号作为类风湿关节炎的治疗靶点:体外和体内的JAK抑制剂

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摘要

Various intercellular signaling plays a pivotal role in the processes of multiple inflammatory diseases, some of which are mediated by soluble ligands such as cytokines and growth factors, and others are mediated by cognate interactions through costimulatory molecules and adhesion molecules. Rheumatoid arthritis (RA) is a representative autoimmune disease characterized with systemic, chronic and destructive inflammatory synovitis and multiple organ manifestations that cause severe disability and mortality in patients. The importance of inflammatory cytokines in the pathogenesis of RA has become apparent from the clinical efficacies of biological agents targeting TNF and IL-6 [1-3]. For such cytokines to exert their biological activities, the appropriate intracellular signaling pathways must be activated by the engagement of their specific receptors on the cell surface, that is outside to in signaling.
机译:多种细胞间信号传导在多种炎性疾病的过程中起着关键作用,其中一些由可溶性配体(例如细胞因子和生长因子)介导,而其他则由通过共刺激分子和粘附分子的同源相互作用介导。类风湿关节炎(RA)是一种典型的自身免疫性疾病,其特征是全身性,慢性和破坏性炎症性滑膜炎以及多处器官表现,导致患者严重残疾和死亡。从针对TNF和IL-6的生物制剂的临床疗效来看,炎症细胞因子在RA发病机理中的重要性已变得显而易见[1-3]。为了使这种细胞因子发挥其生物学活性,必须通过其特异性受体在细胞表面上的参与来激活适当的细胞内信号传导途径,即在信号传导之外。

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