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核因子κB与类风湿关节炎:对遗传风险的理解会带来治疗回报吗?

NF-κB and Rheumatoid Arthritis: Will Understanding Genetic Risk Lead to a Therapeutic Reward?

作者信息

Scheinman Robert

机构信息

University of Colorado Denver, School of Pharmacy, Department of Pharmaceutical Sciences, Aurora, CO 80045;

出版信息

For Immunopathol Dis Therap. 2013 Apr 1;4(2):93-110. doi: 10.1615/ForumImmunDisTher.2013008408.

DOI:10.1615/ForumImmunDisTher.2013008408
PMID:24678426
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3963006/
Abstract

NF-κB has long been known to play an important role in autoimmune diseases such as rheumatoid arthritis (RA). Indeed, as our understanding of how NF-κB is utilized has increased, we have been hard put to find a process not associated with this transcription factor family in some way. However, new data originating, in part, from genome-wide association studies have demonstrated that very specific alterations in components of the NF-κB pathway are sufficient to confer increased risk of developing disease. Here we review the data which have identified specific components of the NF-κB pathway, and consider what is known of their mechanisms of action and how these mechanisms might play into the disease process. In addition, the use of genetic information to predict RA is considered.

摘要

长期以来,人们一直认为核因子-κB(NF-κB)在类风湿性关节炎(RA)等自身免疫性疾病中发挥着重要作用。事实上,随着我们对NF-κB作用方式的理解不断加深,我们很难找到一个与这个转录因子家族毫无关联的过程。然而,部分源于全基因组关联研究的新数据表明,NF-κB信号通路成分的非常特定的改变足以增加患疾病的风险。在此,我们回顾了已确定NF-κB信号通路特定成分的数据,并思考了它们的作用机制以及这些机制如何影响疾病进程。此外,还考虑了利用遗传信息来预测RA的情况。

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本文引用的文献

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CD40 mediates downregulation of CD32B on specific memory B cell populations in rheumatoid arthritis.CD40 介导类风湿关节炎中特定记忆 B 细胞群体上 CD32B 的下调。
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Paeoniflorin Antagonizes TNF-α-Induced L929 Fibroblastoma Cells Apoptosis by Inhibiting NF-κBp65 Activation.芍药苷通过抑制NF-κBp65激活拮抗TNF-α诱导的L929成纤维细胞瘤细胞凋亡。
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Jatrorrhizine Hydrochloride Suppresses Proliferation, Migration, and Secretion of Synoviocytes In Vitro and Ameliorates Rat Models of Rheumatoid Arthritis In Vivo.盐酸小檗碱体外抑制滑膜细胞增殖、迁移和分泌,并在体内改善类风湿关节炎大鼠模型。
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