CD73在自身免疫性关节炎中的作用

P. Chrobak, J. Stagg
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引用次数: 0

摘要

腺苷是一种有效的抗炎分子,在许多疾病中起着重要作用。胞外腺苷水平由膜转运蛋白和外核苷酸酶(如CD73)共同决定。靶向治疗腺苷能通路,如腺苷受体激动剂,可能是治疗类风湿性关节炎(RA)的一种有价值的方法。直到最近,CD73在RA发病机制中的作用尚未确定。使用CD73缺陷基因靶向小鼠,我们证明CD73在小鼠胶原诱导关节炎(CIA)中起关键的保护作用。我们的发现以及最近发表的人类研究结果表明,增强CD73活性可能是治疗RA的一种新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CD73 in Autoimmune Arthritis
Abstract Adenosine is a potent anti-inflammatory molecule that plays an important role in many diseases. Extracellular levels of adenosine are determined by a combination of membrane transporters and ecto-nucleotidases such as CD73. Therapeutic targeting of the adenosinergic pathway, such as administration of adenosine receptor agonists, could be a valuable approach in the treatment of rheumatoid arthritis(RA). Until recently, the role of CD73 in RA pathogenesis had not been established. Using CD73-deficient gene-targeted mice, we demonstrated that CD73 plays a critical protective role in collagen-induced arthritis (CIA) in mice. Our findings, together with the results of recently published human studies, thus suggests that enhancement of CD73 activity may be a novel therapeutic approach in RA.
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