Cutting edge:: Monarch-1 suppresses non-canonical NF-κB activation and p52-dependent chemokine expression in monocytes

被引：174

作者：

Lich, John D. ^{[1
]}

Williams, Kristi L. ^{[1
]}

Moore, Chris B. ^{[1
]}

Arthur, Janelle C. ^{[1
]}

Davis, Beckley K. ^{[1
]}

Taxman, Debra J. ^{[1
]}

Ting, Jenny P-Y ^{[1
]}

机构：

[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA

来源：

JOURNAL OF IMMUNOLOGY | 2007年 / 178卷 / 03期

关键词：

D O I：

10.4049/jimmunol.178.3.1256

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

CATERPILLER (NOD, NBD-LRR) proteins are rapidly emerging as important mediators of innate and adaptive immunity. Among these, Monarch-1 operates as a novel attenuating factor of inflammation by suppressing inflammatory responses in activated monocytes. However, the molecular mechanisms by which Monarch-1 performs this important function are not well understood. In this report, we show that Monarch-1 inhibits CD40-mediated activation of NF-kappa B via the non-canonical pathway in human monocytes. This inhibition stems from the ability of Monarch-1 to associate with and induce proteasome-mediated degradation of NF-kappa B inducing kinase. Congruently, silencing Monarch-1 with shRNA enhances the expression of p52-dependent chemokines.

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收藏

页码：1256 / 1260

页数：5

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