Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways

被引:132
作者
Murray, Peter J. [1 ,2 ]
Smale, Stephen T. [3 ]
机构
[1] St Jude Childrens Res Hosp, Dept Infect Dis, Memphis, TN 38105 USA
[2] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA
[3] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA
基金
美国国家卫生研究院;
关键词
NF-KAPPA-B; TOLL-LIKE RECEPTORS; GENE-SPECIFIC CONTROL; ANTIINFLAMMATORY RESPONSE; SOCS PROTEINS; PROTECTS MICE; ACTIVATION; EXPRESSION; CYTOKINE; TRANSCRIPTION;
D O I
10.1038/ni.2391
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Activation of Toll-like receptor (TLR) signaling and related pathways by microbial products drives inflammatory responses, host-defense pathways and adaptive immunity. The cost of excessive inflammation is cell and tissue damage, an underlying cause of many acute and chronic diseases. Coincident with activation of TLR signaling, a plethora of anti-inflammatory pathways and mechanisms begin to modulate inflammation until tissue repair is complete. Whereas most studies have focused on the signaling components immediately downstream of the TLRs, this Review summarizes the different levels of anti-inflammatory pathways that have evolved to abate TLR signaling and how they are integrated to prevent cell and tissue destruction.
引用
收藏
页码:916 / 924
页数:9
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