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通过相互依存的负调控途径层来抑制炎症信号。

Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways.

机构信息

Department of Infectious Diseases and Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

出版信息

Nat Immunol. 2012 Oct;13(10):916-24. doi: 10.1038/ni.2391. Epub 2012 Sep 18.

Abstract

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.

摘要

Toll 样受体(TLR)信号及其相关途径的激活可被微生物产物驱动,从而引发炎症反应、宿主防御途径和适应性免疫。过度炎症的代价是细胞和组织损伤,这是许多急性和慢性疾病的根本原因。与 TLR 信号的激活同时发生的是,大量的抗炎途径和机制开始调节炎症,直到组织修复完成。虽然大多数研究都集中在 TLR 下游的信号成分上,但本综述总结了进化而来的不同水平的抗炎途径,以减轻 TLR 信号,并探讨它们是如何整合以防止细胞和组织破坏的。

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