The role of uric acid as an endogenous danger signal in immunity and inflammation.
The role of uric acid as an endogenous danger signal in immunity and inflammation.
复制标题
DOI：
10.1007/s11926-011-0162-1
复制
发表时间：
2011-04
影响因子：
5
通讯作者：
Shi, Yan
中科院分区：
文献类型：
--
作者：
Ghaemi-Oskouie, Faranak;Shi, Yan
痛风是一种古老的疾病，至今仍然困扰着我们。其致病元凶，是尿酸结晶沉积在组织中，是一种强烈的炎症兴奋剂。近年来，尿酸晶体促进炎症的机制已成为风湿病学家和免疫学家日益关注的课题。尿酸已被确定为一种内源性佐剂，可在没有微生物刺激的情况下驱动免疫反应。由于尿酸是一种普遍存在的代谢物，在细胞损伤时会大量产生，因此其对健康和疾病的影响可能相当大。尿酸晶体还被证明可以通过激活 NOD 样受体蛋白 (NLRP)3 炎性体（一种多分子复合物，其激活似乎是许多病理性炎症病症的核心）来触发白细胞介素 1β 介导的炎症。在本文中，我们回顾了尿酸介导的炎症的可能机制，并就相对简单物质的复杂作用的了解提供了一些历史观点。
Gout is an ancient disease that still plagues us. Its pathogenic culprit, uric acid crystal deposition in tissues, is a strong inflammatory stimulant. In recent years, the mechanisms through which uric acid crystals promote inflammation have been a subject of increasing interest among rheumatologists and immunologists. Uric acid has been identified as an endogenous adjuvant that drives immune responses in the absence of microbial stimulation. Because uric acid is a ubiquitous metabolite that is produced in high quantities upon cellular injury, the ramifications of its effects may be considerable in health and in disease. Uric acid crystals also have been shown to trigger interleukin-1β–mediated inflammation via activation of the NOD-like receptor protein (NLRP)3 inflammasome, a multimolecular complex whose activation appears to be central to many pathological inflammatory conditions. In this article, we review the possible mechanisms of uric acid–mediated inflammation and offer some historical perspectives on what has been learned about the complex effects of a relatively simple substance.
登录
查看更多内容
影响因子：
6.6
作者：
IWATA, H;NISHIO, S;TAKEUCHI, M
通讯作者：
TAKEUCHI, M
影响因子：
82.9
作者：
Chen, Chun-Jen;Kono, Hajime;Rock, Kenneth L.
通讯作者：
Rock, Kenneth L.
影响因子：
64.8
作者：
Enomoto, A;Kimura, H;Endou, H
通讯作者：
Endou, H
影响因子：
30.5
作者：
通讯作者：
--
影响因子：
4.4
作者：
Kool, Mirjam;Petrilli, Virginie;Tschopp, Juerg
通讯作者：
Tschopp, Juerg