Toll-like receptor (TLR) and inflammasome actions in the central nervous system

被引：170

作者：

Hanamsagar, Richa ^{[2
]}

Hanke, Mark L. ^{[1
]}

Kielian, Tammy ^{[1
]}

机构：

[1] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA

[2] Univ Nebraska, Med Ctr, Dept Pharmacol & Expt Neurosci, Omaha, NE 68198 USA

来源：

TRENDS IN IMMUNOLOGY | 2012年 / 33卷 / 07期

关键词：

inflammasome; Toll-like receptor; microglia; IL-1; beta; IL-18; neurodegeneration; bacterial meningitis; brain abscess; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; HOST IMMUNE-RESPONSE; EXPERIMENTAL PNEUMOCOCCAL MENINGITIS; EXPERIMENTAL BRAIN-ABSCESS; SPINAL-CORD-INJURY; SPECK-LIKE PROTEIN; NALP3; INFLAMMASOME; INNATE IMMUNITY; ALZHEIMERS-DISEASE; MULTIPLE-SCLEROSIS;

D O I：

10.1016/j.it.2012.03.001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

During the past 10 years, much attention has been focused towards elucidating the impact of Toll-like receptors (TLRs) in central nervous system (CNS) innate immunity. TLR signaling triggers the transcriptional activation of pro-interleukin-1 beta (pro-IL-1 beta) and pro-IL-18 that are processed into their active forms by the inflammasome. Recent studies have demonstrated inflammasome involvement during CNS infection, autoimmune disease, and injury. This review will address inflammasome actions within the CNS and how cooperation between TLR and inflammasome signaling may influence disease outcome. In addition, the concept of alternative inflammasome functions independent of IL-1 and IL-18 processing are considered in the context of CNS disease.

引用

页码：333 / 342

页数：10

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