期刊
CURRENT OPINION IN RHEUMATOLOGY
卷 19, 期 2, 页码 146-150出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0b013e328014529a
关键词
inflammasome; innate immunity; nuclear hormone receptors; Toll-like receptors; TREM-1
类别
Purpose of review The aim of this article is to highlight recent advances suggesting essential involvement of the innate immune system in crystal-induced acute inflammation. Recent findings Gout is a disease caused by the deposition of monosodium urate monohydrate crystals. Precise mechanisms underlying the initiation of monosodium urate monohydrate crystal-induced acute inflammation, however, are not known. Recent investigations provided novel evidence in the pathology of acute gout. Immunological study indicated that monosodium urate monohydrate crystals can act as a 'danger signal' that resembles exogenous adjuvants. Two laboratories have documented interesting findings that Toll-like receptor-mediated pathways or MyD88-dependent pathways are involved in monosodium urate monohydrate crystal-induced acute inflammation. Upregulation of the triggering receptor expressed on myeloid cells 1 (TREM-1) in phagocytes by the stimulation with monosodium urate monohydrate crystals has been demonstrated. Furthermore, pathological significance of NALP 3 inflammasome in gout has been shown. These findings provide a new concept that the innate immune system may play a crucial role on the triggering of crystal-induced acute inflammation. Spontaneous resolution is a characteristic feature of acute gout. Involvement of nuclear hormone receptors, peroxisome proliferator-activated receptor gamma and liver X receptor alpha, during the termination of acute gout has been also shown. Summary These studies provided a new insight into the mechanisms underlying the initiation and the termination of monosodium urate monohydrate crystal-induced acute inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据